Question:medium
Male not responding to O₂, diagnosis ARDS. What is the role of IL-8 in ARDS?
Male not responding to O₂, diagnosis ARDS. What is the role of IL-8 in ARDS?
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IL-8 (CXCL8) is the classic chemokine that calls in one specific leukocyte — think which cell does the alveolar damage in ARDS.
Updated On: Jun 22, 2026
- Endothelial cell activation
- Requirement of neutrophil
- Macrophage activation
- Promote surfactant production
Show Solution
The Correct Option is B
Solution and Explanation
Mechanism-first approach.
Start from the question "what is the single defining function of IL-8?" IL-8 belongs to the CXC chemokine family. CXC chemokines with the ELR motif are specialised to attract neutrophils. So before considering ARDS at all, IL-8 = neutrophil chemoattractant.
Applying it to ARDS.
ARDS injury is fundamentally neutrophil-mediated. Activated alveolar macrophages and injured epithelium pour out IL-8 into the alveoli. This IL-8 gradient pulls neutrophils across the capillary endothelium into the air spaces, where they degranulate and release elastase and oxidants, tearing the alveolar-capillary membrane. The result is leaky, protein-rich edema and the refractory hypoxia that does not improve with oxygen alone.
Therefore the link being tested.
IL-8 is required to bring neutrophils to the lung - matching "requirement of neutrophil." ($answer = B$)
Eliminating distractors.
Endothelial activation → TNF-α / IL-1 territory, not IL-8.
Macrophage activation → macrophages secrete IL-8; they are the source, not the recipient, and activation is an IFN-γ phenomenon.
Surfactant production → a type-II pneumocyte function that is lost in ARDS, never promoted by a pro-inflammatory chemokine.
Conclusion: IL-8 drives neutrophil recruitment - Option B.
Start from the question "what is the single defining function of IL-8?" IL-8 belongs to the CXC chemokine family. CXC chemokines with the ELR motif are specialised to attract neutrophils. So before considering ARDS at all, IL-8 = neutrophil chemoattractant.
Applying it to ARDS.
ARDS injury is fundamentally neutrophil-mediated. Activated alveolar macrophages and injured epithelium pour out IL-8 into the alveoli. This IL-8 gradient pulls neutrophils across the capillary endothelium into the air spaces, where they degranulate and release elastase and oxidants, tearing the alveolar-capillary membrane. The result is leaky, protein-rich edema and the refractory hypoxia that does not improve with oxygen alone.
Therefore the link being tested.
IL-8 is required to bring neutrophils to the lung - matching "requirement of neutrophil." ($answer = B$)
Eliminating distractors.
Endothelial activation → TNF-α / IL-1 territory, not IL-8.
Macrophage activation → macrophages secrete IL-8; they are the source, not the recipient, and activation is an IFN-γ phenomenon.
Surfactant production → a type-II pneumocyte function that is lost in ARDS, never promoted by a pro-inflammatory chemokine.
Conclusion: IL-8 drives neutrophil recruitment - Option B.
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