Microbiology Quiz: Inflammation And Phagocytosis
20 questions · exam conditions
0:00
Inflammation And PhagocytosisQuestion 1 of 20

A tissue biopsy is taken from a site of inflammation. Histological analysis reveals a predominant infiltrate of lymphocytes and macrophages, along with evidence of fibrosis and tissue remodeling. This cellular profile is most characteristic of which condition?

The initial 4 hours of an acute bacterial infection.
An immediate hypersensitivity reaction (Type I).
The resolution phase of acute inflammation.
Chronic inflammation.
← Back to quizzes

Microbiology Quiz

Microbiology Quiz: Inflammation And Phagocytosis

Practice Inflammation And Phagocytosis in Microbiology with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.

What this quiz covers

This quiz focuses on Inflammation And Phagocytosis, giving you a quick way to practice the rules, question types, and explanations that matter most for Microbiology.

How to use this quiz

Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

All questions

Question 1

A tissue biopsy is taken from a site of inflammation. Histological analysis reveals a predominant infiltrate of lymphocytes and macrophages, along with evidence of fibrosis and tissue remodeling. This cellular profile is most characteristic of which condition?

  1. The initial 4 hours of an acute bacterial infection.
  2. An immediate hypersensitivity reaction (Type I).
  3. The resolution phase of acute inflammation.
  4. Chronic inflammation. (correct answer)
Explanation: The correct answer is D. Chronic inflammation is characterized by a persistent inflammatory stimulus, leading to a different cellular infiltrate than acute inflammation. The hallmark cells of chronic inflammation are mononuclear cells, including macrophages, lymphocytes (T and B cells), and plasma cells. This persistent inflammation often occurs alongside attempts at repair, leading to fibrosis (scarring) and tissue remodeling. A: The initial phase of acute inflammation is dominated by neutrophils. B: Type I hypersensitivity reactions are characterized by mast cells, eosinophils, and edema. C: The resolution phase would show declining numbers of inflammatory cells, primarily apoptotic neutrophils being cleared by macrophages, not a heavy infiltrate of lymphocytes and fibrosis.

Question 2

A patient with a rare genetic disorder presents with recurrent bacterial infections. Laboratory analysis reveals their neutrophils can successfully engulf opsonized Staphylococcus aureus but fail to kill the internalized bacteria. Further investigation shows that while lysosomes are present and functional, they do not fuse with the bacteria-containing vacuoles. This defect is most analogous to the pathogenic evasion mechanism employed by which microorganism?

  1. Staphylococcus aureus
  2. Streptococcus pneumoniae
  3. Listeria monocytogenes
  4. Mycobacterium tuberculosis (correct answer)
Explanation: The correct answer is D. Mycobacterium tuberculosis is a classic example of an intracellular pathogen that survives within phagocytes by actively inhibiting the fusion of the phagosome with the lysosome, thereby preventing the formation of a microbicidal phagolysosome. The genetic defect described in the patient mirrors this specific survival strategy. A: Staphylococcus aureus is the bacterium used in the experimental setup, but its primary survival mechanisms involve producing catalase to resist oxidative killing and toxins, not inhibiting phagolysosome fusion. B: Streptococcus pneumoniae primarily evades the immune system by possessing a polysaccharide capsule that prevents phagocytic uptake in the first place. C: Listeria monocytogenes survives phagocytosis by producing listeriolysin O, an enzyme that lyses the phagosomal membrane, allowing the bacterium to escape into the host cell's cytoplasm.

Question 3

An unresolved bacterial infection in a patient's liver has led to the formation of an abscess. This outcome of acute inflammation represents a 'frustrated' healing process. Which statement best describes the central feature of an abscess that limits both immune cell function and antibiotic penetration?

  1. An area of uncontrolled vasodilation and vascular permeability leading to massive edema.
  2. A central core of necrotic tissue, dead neutrophils (pus), and bacteria surrounded by a fibrous capsule. (correct answer)
  3. A predominant infiltration of T lymphocytes and plasma cells secreting high levels of antibody.
  4. Rapid and complete clearance of the pathogen followed by extensive scar tissue formation.
Explanation: The correct answer is B. An abscess is the result of the body's attempt to wall off an infection that it cannot clear. It is characterized by a central region of pus, which is composed of dead neutrophils, liquefied necrotic tissue, and the infectious organisms. This core is typically surrounded by a fibrous capsule formed by fibroblasts. This structure creates an avascular, acidic, and anaerobic environment that is difficult for additional immune cells and systemically administered antibiotics to penetrate, allowing the infection to persist. A: This describes the early stages of acute inflammation, not the organized structure of an abscess. C: This cellular profile is more characteristic of certain types of chronic inflammation, not a typical purulent abscess. D: This describes successful resolution with repair, which is the opposite of an abscess.

Question 4

A patient has a genetic deficiency in the receptor for the complement component C5a. While other parts of the complement cascade are intact, allowing formation of the membrane attack complex (MAC), which specific function of the inflammatory response would be most severely impaired?

  1. Opsonization of bacteria by C3b deposition.
  2. Direct lysis of Gram-negative bacteria by the MAC.
  3. Histamine release from mast cells mediated by anaphylatoxins.
  4. Chemotactic recruitment of neutrophils to the site of infection. (correct answer)
Explanation: The correct answer is D. C5a is the most potent chemotactic factor generated by the complement system. It creates a powerful chemical gradient that attracts phagocytes, particularly neutrophils, to the site of complement activation. A defect in the C5a receptor would severely impair this crucial recruitment step. A: C3b is the primary opsonin of the complement system, and its generation occurs upstream of C5a cleavage. This process would be intact. B: The MAC (C5b-9) forms from components downstream of C5 cleavage. Since the cascade is otherwise intact, MAC formation would still occur. C: While C5a is an anaphylatoxin that can trigger histamine release, C3a also has this function. Therefore, this capability would be diminished but not completely lost, unlike the potent chemotactic signal of C5a.

Question 5

During a bacterial infection, macrophage recognition of PAMPs leads to the release of TNF-α. This cytokine then acts on local endothelial cells. Which of the following pairs of events is a direct downstream consequence of TNF-α signaling on the endothelium?

  1. Decreased blood flow and decreased expression of ICAM-1.
  2. Increased expression of E-selectin and increased vascular permeability. (correct answer)
  3. Mast cell degranulation and activation of the alternative complement pathway.
  4. Systemic fever induction and chemotaxis of neutrophils.
Explanation: The correct answer is B. TNF-α is a potent activator of endothelial cells. Its local effects include inducing the expression of adhesion molecules, such as E-selectin (for leukocyte rolling) and ICAM-1 (for firm adhesion). TNF-α also acts on the endothelial junctions, increasing vascular permeability, which allows plasma proteins and fluid to enter the tissue, causing edema. A: TNF-α causes vasodilation, which increases local blood flow, and it increases, not decreases, the expression of ICAM-1. C: These are not direct effects of TNF-α on endothelial cells. Mast cell degranulation and complement activation are triggered by other signals. D: Fever is a systemic effect of TNF-α acting on the hypothalamus, not a local effect on the endothelium. Chemotaxis is primarily driven by chemokines, although TNF-α does induce chemokine production.

Question 6

A researcher is studying a strain of neutrophils that have a functional NADPH oxidase but lack the gene for lysozyme. These neutrophils would be most specifically deficient in their ability to kill which type of bacteria and by what mechanism?

  1. Gram-positive bacteria, by degrading their peptidoglycan cell wall. (correct answer)
  2. Gram-negative bacteria, by disrupting their outer membrane with the MAC.
  3. All bacteria, by generating hypochlorous acid from hydrogen peroxide.
  4. Intracellular bacteria, by preventing their escape from the phagosome.
Explanation: The correct answer is A. Lysozyme is an enzyme found in phagocytic granules that specifically targets and degrades peptidoglycan, a major component of bacterial cell walls. Gram-positive bacteria have a very thick, exposed peptidoglycan layer, making them particularly susceptible to lysozyme. While Gram-negative bacteria also have peptidoglycan, it is much thinner and located beneath an outer membrane. Therefore, a deficiency in lysozyme would most specifically impair an oxygen-independent killing mechanism against Gram-positive bacteria. B: The MAC is part of the complement system, not a direct tool of the neutrophil's internal killing machinery. C: The generation of hypochlorous acid (bleach) requires the enzyme myeloperoxidase (MPO) and the products of the respiratory burst (which is intact). This is a separate mechanism from lysozyme action. D: Lysozyme does not prevent bacterial escape from the phagosome.

Question 7

Both neutrophils and macrophages are professional phagocytes crucial for controlling bacterial infections. A key functional difference is that after phagocytosing a pathogen, macrophages are uniquely equipped to perform which of the following actions to a significant extent?

  1. Undergo a respiratory burst to produce reactive oxygen species.
  2. Present processed antigens on MHC class II molecules to T helper cells. (correct answer)
  3. Release cytokines and chemokines to recruit additional immune cells.
  4. Migrate from the bloodstream into infected tissues via diapedesis.
Explanation: The correct answer is B. While both cell types are phagocytes, macrophages also function as professional antigen-presenting cells (APCs). After engulfing and digesting a pathogen, macrophages process its antigens and present peptide fragments on Major Histocompatibility Complex (MHC) class II molecules on their surface. This presentation is essential for activating naive T helper cells and initiating an adaptive immune response. Neutrophils are not considered significant APCs. A: Both neutrophils and macrophages perform a respiratory burst, although it is typically more potent in neutrophils. C: Both cell types release a variety of cytokines and chemokines to orchestrate the immune response. D: Both cell types are recruited from the blood and migrate into tissues in response to infection.

Question 8

A patient with a rare genetic disorder presents with recurrent bacterial infections. Laboratory analysis reveals their neutrophils can successfully engulf opsonized Staphylococcus aureus but fail to kill the internalized bacteria. Further investigation shows that while lysosomes are present and functional, they do not fuse with the bacteria-containing vacuoles. This defect is most analogous to the pathogenic evasion mechanism employed by which microorganism?

  1. Staphylococcus aureus
  2. Streptococcus pneumoniae
  3. Listeria monocytogenes
  4. Mycobacterium tuberculosis (correct answer)
Explanation: The correct answer is D. Mycobacterium tuberculosis is a classic example of an intracellular pathogen that survives within phagocytes by actively inhibiting the fusion of the phagosome with the lysosome, thereby preventing the formation of a microbicidal phagolysosome. The genetic defect described in the patient mirrors this specific survival strategy. A: Staphylococcus aureus is the bacterium used in the experimental setup, but its primary survival mechanisms involve producing catalase to resist oxidative killing and toxins, not inhibiting phagolysosome fusion. B: Streptococcus pneumoniae primarily evades the immune system by possessing a polysaccharide capsule that prevents phagocytic uptake in the first place. C: Listeria monocytogenes survives phagocytosis by producing listeriolysin O, an enzyme that lyses the phagosomal membrane, allowing the bacterium to escape into the host cell's cytoplasm.

Question 9

A macrophage has just engulfed a bacterium. The subsequent activation of the NADPH oxidase complex is a critical step for bacterial killing. What is the immediate biochemical consequence of this enzyme's activity at the phagosomal membrane?

  1. Generation of superoxide anions (O₂⁻) in the phagosome lumen. (correct answer)
  2. Release of myeloperoxidase from granules into the cytoplasm.
  3. Consumption of nitric oxide to form peroxynitrite radicals.
  4. Fusion of the phagosome with a lysosome to form a phagolysosome.
Explanation: The correct answer is A. The NADPH oxidase complex, located in the phagosome membrane, catalyzes the transfer of an electron from NADPH (in the cytoplasm) to molecular oxygen (O₂) within the phagosome lumen. This one-electron reduction of oxygen is the immediate first step of the respiratory burst, producing the superoxide anion (O₂⁻), a highly reactive oxygen species. B: Myeloperoxidase is released from azurophilic granules into the phagolysosome (not the cytoplasm) where it acts on hydrogen peroxide, a downstream product of the respiratory burst. C: Peroxynitrite formation requires nitric oxide, which is generated by a different enzyme, inducible nitric oxide synthase (iNOS), not NADPH oxidase. D: Phagolysosome fusion is a separate, albeit often concurrent, cellular process involving membrane trafficking, not a direct biochemical product of NADPH oxidase activity.

Question 10

A strain of Streptococcus pneumoniae has a thick polysaccharide capsule that is poorly recognized by macrophage pattern recognition receptors (PRRs). However, an adaptive immune response has produced specific IgG antibodies against the capsule. How does the presence of this specific IgG most directly facilitate phagocytosis of the bacterium?

  1. By activating the alternative complement pathway, leading to C3b deposition.
  2. By neutralizing bacterial toxins, allowing the phagocyte to approach safely.
  3. By binding to Fcγ receptors on the macrophage, bridging the bacterium to the phagocyte. (correct answer)
  4. By directly triggering Toll-like receptors to enhance phagosome maturation.
Explanation: The correct answer is C. IgG antibodies act as opsonins. Their Fab (Fragment antigen-binding) regions bind to antigens on the bacterial surface (the capsule in this case), while their Fc (Fragment crystallizable) portion is recognized by Fcγ receptors on the surface of phagocytes like macrophages. This binding creates a molecular bridge that directly links the bacterium to the phagocyte, triggering engulfment. A: IgG activates the classical complement pathway, not the alternative pathway. While this does lead to C3b deposition (another opsonin), the most direct action of the IgG molecule itself is via Fc receptors. B: While antibody neutralization of toxins is a protective mechanism, it does not directly facilitate the physical process of phagocytosis. D: Toll-like receptors (TLRs) recognize conserved microbial structures (PAMPs), not the Fc portion of host antibodies.

Question 11

Both neutrophils and macrophages are professional phagocytes crucial for controlling bacterial infections. A key functional difference is that after phagocytosing a pathogen, macrophages are uniquely equipped to perform which of the following actions to a significant extent?

  1. Undergo a respiratory burst to produce reactive oxygen species.
  2. Present processed antigens on MHC class II molecules to T helper cells. (correct answer)
  3. Release cytokines and chemokines to recruit additional immune cells.
  4. Migrate from the bloodstream into infected tissues via diapedesis.
Explanation: The correct answer is B. While both cell types are phagocytes, macrophages also function as professional antigen-presenting cells (APCs). After engulfing and digesting a pathogen, macrophages process its antigens and present peptide fragments on Major Histocompatibility Complex (MHC) class II molecules on their surface. This presentation is essential for activating naive T helper cells and initiating an adaptive immune response. Neutrophils are not considered significant APCs. A: Both neutrophils and macrophages perform a respiratory burst, although it is typically more potent in neutrophils. C: Both cell types release a variety of cytokines and chemokines to orchestrate the immune response. D: Both cell types are recruited from the blood and migrate into tissues in response to infection.

Question 12

The binding of lipopolysaccharide (LPS) from a Gram-negative bacterium to Toll-like receptor 4 (TLR4) on a macrophage initiates a signaling cascade. Besides inducing the production of inflammatory cytokines, what is another critical, direct outcome of this TLR signaling for the phagocytic process?

  1. It triggers the immediate release of pre-formed histamine granules.
  2. It serves as the primary opsonin, directly coating the bacterial surface.
  3. It promotes phagosome maturation and enhances fusion with lysosomes. (correct answer)
  4. It activates the classical complement pathway on the macrophage surface.
Explanation: The correct answer is C. TLR signaling is not just about producing external signals like cytokines. It also initiates intracellular programs that enhance the killing of phagocytosed microbes. TLR signaling pathways promote the maturation of the phagosome, including its acidification and fusion with lysosomes to form the highly microbicidal phagolysosome. This directly links pathogen recognition to enhanced intracellular killing. A: Macrophages do not store histamine in granules; this is characteristic of mast cells and basophils. B: TLR4 is a signaling receptor on the macrophage, not an opsonin that coats bacteria. Opsonins include C3b and IgG. D: The classical complement pathway is activated by antigen-antibody complexes, not directly by TLR signaling on the macrophage.

Question 13

An unresolved bacterial infection in a patient's liver has led to the formation of an abscess. This outcome of acute inflammation represents a 'frustrated' healing process. Which statement best describes the central feature of an abscess that limits both immune cell function and antibiotic penetration?

  1. An area of uncontrolled vasodilation and vascular permeability leading to massive edema.
  2. A central core of necrotic tissue, dead neutrophils (pus), and bacteria surrounded by a fibrous capsule. (correct answer)
  3. A predominant infiltration of T lymphocytes and plasma cells secreting high levels of antibody.
  4. Rapid and complete clearance of the pathogen followed by extensive scar tissue formation.
Explanation: The correct answer is B. An abscess is the result of the body's attempt to wall off an infection that it cannot clear. It is characterized by a central region of pus, which is composed of dead neutrophils, liquefied necrotic tissue, and the infectious organisms. This core is typically surrounded by a fibrous capsule formed by fibroblasts. This structure creates an avascular, acidic, and anaerobic environment that is difficult for additional immune cells and systemically administered antibiotics to penetrate, allowing the infection to persist. A: This describes the early stages of acute inflammation, not the organized structure of an abscess. C: This cellular profile is more characteristic of certain types of chronic inflammation, not a typical purulent abscess. D: This describes successful resolution with repair, which is the opposite of an abscess.

Question 14

Inflammation can be initiated in the absence of any microbial pathogen, a process known as sterile inflammation. In this scenario, what type of molecule, released from stressed or necrotic host cells, is responsible for triggering the inflammatory response by engaging pattern recognition receptors?

  1. Pathogen-associated molecular patterns (PAMPs).
  2. Damage-associated molecular patterns (DAMPs). (correct answer)
  3. Opsonins, such as C3b and IgG.
  4. Endogenous pyrogens, such as IL-1.
Explanation: The correct answer is B. Damage-associated molecular patterns (DAMPs), also known as alarmins, are endogenous molecules released from damaged, stressed, or dying host cells. Examples include ATP, uric acid crystals, and high-mobility group box 1 (HMGB1). These molecules signal to the immune system that tissue damage has occurred, and they are recognized by pattern recognition receptors (PRRs), similar to how PAMPs are recognized, initiating an inflammatory response even without an infection. A: PAMPs are conserved molecular structures found on microorganisms and are, by definition, absent in sterile inflammation. C: Opsonins are part of the downstream inflammatory response; they mark targets for phagocytosis but do not initiate sterile inflammation. D: Endogenous pyrogens like IL-1 are cytokines produced during the inflammatory response; they are a consequence, not the initial trigger, of DAMP recognition.

Question 15

The binding of lipopolysaccharide (LPS) from a Gram-negative bacterium to Toll-like receptor 4 (TLR4) on a macrophage initiates a signaling cascade. Besides inducing the production of inflammatory cytokines, what is another critical, direct outcome of this TLR signaling for the phagocytic process?

  1. It triggers the immediate release of pre-formed histamine granules.
  2. It serves as the primary opsonin, directly coating the bacterial surface.
  3. It promotes phagosome maturation and enhances fusion with lysosomes. (correct answer)
  4. It activates the classical complement pathway on the macrophage surface.
Explanation: The correct answer is C. TLR signaling is not just about producing external signals like cytokines. It also initiates intracellular programs that enhance the killing of phagocytosed microbes. TLR signaling pathways promote the maturation of the phagosome, including its acidification and fusion with lysosomes to form the highly microbicidal phagolysosome. This directly links pathogen recognition to enhanced intracellular killing. A: Macrophages do not store histamine in granules; this is characteristic of mast cells and basophils. B: TLR4 is a signaling receptor on the macrophage, not an opsonin that coats bacteria. Opsonins include C3b and IgG. D: The classical complement pathway is activated by antigen-antibody complexes, not directly by TLR signaling on the macrophage.

Question 16

A patient taking a high dose of a non-steroidal anti-inflammatory drug (NSAID) that selectively inhibits cyclooxygenase-2 (COX-2) sustains a minor tissue injury. Compared to an individual not taking the drug, which aspect of the acute inflammatory response would be most significantly diminished in this patient?

  1. Initial histamine release from mast cells following injury.
  2. Prostaglandin-mediated vasodilation and pain sensitization. (correct answer)
  3. Leukocyte rolling mediated by selectin upregulation on endothelium.
  4. Activation of the alternative complement pathway on microbial surfaces.
Explanation: The correct answer is B. Cyclooxygenase-2 (COX-2) is an enzyme induced during inflammation that is responsible for synthesizing prostaglandins. Prostaglandins are key mediators that cause vasodilation (contributing to redness and heat) and sensitize nerve endings to pain. An NSAID that inhibits COX-2 would therefore most directly and significantly reduce these effects. A: Histamine release is an early event triggered by mast cell degranulation due to injury or other stimuli, occurring upstream of or parallel to the COX pathway. C: The upregulation of selectins on endothelial cells is primarily driven by other cytokines like TNF-α and IL-1, not prostaglandins. D: The alternative complement pathway is typically activated by direct contact with pathogen surfaces and is not dependent on the COX-2 pathway.

Question 17

A macrophage has just engulfed a bacterium. The subsequent activation of the NADPH oxidase complex is a critical step for bacterial killing. What is the immediate biochemical consequence of this enzyme's activity at the phagosomal membrane?

  1. Generation of superoxide anions (O₂⁻) in the phagosome lumen. (correct answer)
  2. Release of myeloperoxidase from granules into the cytoplasm.
  3. Consumption of nitric oxide to form peroxynitrite radicals.
  4. Fusion of the phagosome with a lysosome to form a phagolysosome.
Explanation: The correct answer is A. The NADPH oxidase complex, located in the phagosome membrane, catalyzes the transfer of an electron from NADPH (in the cytoplasm) to molecular oxygen (O₂) within the phagosome lumen. This one-electron reduction of oxygen is the immediate first step of the respiratory burst, producing the superoxide anion (O₂⁻), a highly reactive oxygen species. B: Myeloperoxidase is released from azurophilic granules into the phagolysosome (not the cytoplasm) where it acts on hydrogen peroxide, a downstream product of the respiratory burst. C: Peroxynitrite formation requires nitric oxide, which is generated by a different enzyme, inducible nitric oxide synthase (iNOS), not NADPH oxidase. D: Phagolysosome fusion is a separate, albeit often concurrent, cellular process involving membrane trafficking, not a direct biochemical product of NADPH oxidase activity.

Question 18

In leukocyte adhesion deficiency type 1 (LAD-1), a defect in the CD18 subunit of β2-integrins prevents leukocytes from adhering firmly to the endothelium. Which of the following events would still occur relatively normally in a patient with LAD-1 during the initial stages of a bacterial infection?

  1. Stable arrest of neutrophils on the vascular endothelium.
  2. Upregulation of E-selectin and transient tethering of neutrophils. (correct answer)
  3. Diapedesis of neutrophils through the endothelial barrier.
  4. Formation of a purulent abscess at the site of infection.
Explanation: The correct answer is B. Leukocyte extravasation is a multi-step process. The initial step involves transient tethering and rolling of leukocytes along the endothelium, which is mediated by selectins on the endothelial cells binding to their ligands on leukocytes. This step precedes firm adhesion. Since LAD-1 affects integrins, which are responsible for firm adhesion, the initial selectin-mediated rolling would still occur. The subsequent steps would be impaired. A: Stable arrest is the step directly mediated by integrins, which are defective in LAD-1, so this would be severely impaired. C: Diapedesis (transmigration) can only occur after stable arrest, so it would also be impaired. D: Abscess formation requires the accumulation of neutrophils at the infection site, which is prevented by the extravasation defect in LAD-1.

Question 19

A patient's neutrophils are found to have a mutation that prevents the acidification of their phagosomes. The pH within the phagosome remains near neutral (pH 7.4) instead of dropping to the typical 4.5-5.0. This defect would most directly impair the function of which class of microbicidal agents?

  1. Reactive oxygen species (ROS) generated by NADPH oxidase.
  2. Cationic peptides (defensins) that disrupt bacterial membranes.
  3. Lysosomal acid hydrolases. (correct answer)
  4. Lactoferrin, which sequesters iron from bacteria.
Explanation: The correct answer is C. Lysosomal enzymes that are delivered to the phagosome to kill and digest microbes are predominantly acid hydrolases. As their name implies, these enzymes, which include proteases, nucleases, and lipases, have optimal activity at the low pH (~4.5-5.0) that is normally established within the phagolysosome. If the phagosome fails to acidify, the activity of these crucial digestive enzymes will be severely impaired. A: The NADPH oxidase enzyme complex actually functions optimally at a neutral pH, so its ability to generate ROS would not be directly inhibited. B and D: While the function of defensins and lactoferrin can be influenced by pH, the class of agents most fundamentally dependent on an acidic environment for their primary function are the acid hydrolases.

Question 20

In leukocyte adhesion deficiency type 1 (LAD-1), a defect in the CD18 subunit of β2-integrins prevents leukocytes from adhering firmly to the endothelium. Which of the following events would still occur relatively normally in a patient with LAD-1 during the initial stages of a bacterial infection?

  1. Stable arrest of neutrophils on the vascular endothelium.
  2. Upregulation of E-selectin and transient tethering of neutrophils. (correct answer)
  3. Diapedesis of neutrophils through the endothelial barrier.
  4. Formation of a purulent abscess at the site of infection.
Explanation: The correct answer is B. Leukocyte extravasation is a multi-step process. The initial step involves transient tethering and rolling of leukocytes along the endothelium, which is mediated by selectins on the endothelial cells binding to their ligands on leukocytes. This step precedes firm adhesion. Since LAD-1 affects integrins, which are responsible for firm adhesion, the initial selectin-mediated rolling would still occur. The subsequent steps would be impaired. A: Stable arrest is the step directly mediated by integrins, which are defective in LAD-1, so this would be severely impaired. C: Diapedesis (transmigration) can only occur after stable arrest, so it would also be impaired. D: Abscess formation requires the accumulation of neutrophils at the infection site, which is prevented by the extravasation defect in LAD-1.