Questions: Acute Inflammation

Question 1

Which of the following best explains why neutrophils are the predominant cell type in the early phase of acute inflammation?

• A. They are the most abundant leukocyte in lymph nodes and are rapidly released
• B. They are rapidly recruited via chemotaxis, arrive first, and are specialized for phagocytosis of debris and pathogens
• C. They produce the antibodies needed to neutralize antigens at the injury site
• D. They are resident tissue cells that transform into phagocytes upon injury

Answer: (B)

Neutrophils are the first responders of acute inflammation. Within hours of injury, chemokines (particularly IL-8/CXCL8) create a gradient that recruits circulating neutrophils through the process of rolling, adhesion, and transmigration. They are highly effective phagocytes capable of engulfing bacteria and debris and releasing reactive oxygen species. Antibody production is an adaptive immune function (B cells/plasma cells), not an innate response.

Question 2

Acute inflammation is exclusively triggered by infection with bacteria or viruses.

• T. True
• F. False

Answer: False

Acute inflammation is a response to tissue injury, which can be caused by infection, physical trauma, burns, ischemia, or chemical irritants — all without any pathogen present. Sterile inflammation (triggered by danger-associated molecular patterns, or DAMPs, released from damaged host cells) activates the same vascular and cellular cascade as infection-driven inflammation. This distinction matters clinically: treating sterile inflammation with antibiotics is ineffective.

Question 3

What is the physiological basis for the five cardinal signs of acute inflammation: rubor, calor, tumor, dolor, and functio laesa?

Model answer: Vasodilation increases local blood flow, causing redness (rubor) and warmth (calor). Increased vascular permeability allows protein-rich fluid to leak into the interstitium, causing swelling/edema (tumor). Inflammatory mediators such as bradykinin and prostaglandin E2 sensitize nociceptors, causing pain (dolor). Edema and pain together impair the tissue's normal mechanical function (functio laesa).

These signs map directly onto the underlying vascular and mediator events. Rubor and calor reflect arteriolar dilation (histamine, prostaglandins). Tumor reflects the exudation of plasma through gaps in post-capillary venule endothelium. Dolor involves both direct stimulation of nociceptors by mediators and lowered thresholds from prostaglandins. Understanding the mediator basis of each sign helps predict which pharmacological interventions (e.g., NSAIDs blocking prostaglandin synthesis) will address which signs.