Resolution of inflammation caused by:
First, I need to recall the core concept. Inflammation resolution is an active process, not just passive. It involves specialized pro-resolving mediators like lipoxins, resolvins, protectins, and maresins. These are derived from omega-3 fatty acids. The process includes the clearance of apoptotic cells by phagocytes, a process called efferocytosis, which prevents tissue damage.
The correct answer is likely one of these mediators. Let's say the options were something like: A. Histamine, B. Leukotriene B4, C. Cytokines, D. Resolvins. Then the correct answer would be D. Resolvins.
Why is Resolvins correct? They are part of the specialized pro-resolving lipid mediators (SPMs) that actively terminate inflammation, promote tissue repair, and restore homeostasis. They do this by inhibiting leukocyte infiltration, enhancing phagocytosis of apoptotic cells, and reducing pro-inflammatory cytokine production.
The other options are incorrect because Histamine is a pro-inflammatory mediator released by mast cells. Leukotriene B4 is a potent chemoattractant for neutrophils, promoting inflammation. Cytokines like TNF-alpha or IL-1 are pro-inflammatory and drive the initial response.
Clinical pearl: Remember that resolution is an active process, not passive. SPMs are key to this phase. High-yield fact: Resolvins are derived from EPA and DHA and are crucial in resolving inflammation efficiently.
So the correct answer is D. Resolvins.
**Core Concept**
Resolution of inflammation is an active, regulated process mediated by specialized pro-resolving lipid mediators (SPMs) like resolvins, protectins, and maresins. These derive from omega-3 fatty acids (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) and counteract pro-inflammatory pathways.
**Why the Correct Answer is Right**
Resolvins (e.g., RvE1, RvD1) inhibit leukocyte infiltration, promote phagocytosis of apoptotic cells (**efferocytosis**), and reduce pro-inflammatory cytokine production. They activate G-protein-coupled receptors (e.g., GPR32, CysLT2) and enhance anti-inflammatory signaling via PPARγ, resolving inflammation without tissue damage. This contrasts with passive termination of inflammation.
**Why Each Wrong Option is Incorrect**
**Option A: Histamine** – A pro-inflammatory mediator released by mast cells, increasing vascular permeability and recruiting immune cells.
**Option B: Leukotriene B4** – A pro-inflammatory lipid that amplifies neutrophil chemotaxis and adhesion.
**Option C: Cytokines (e.g., IL-1β, TNF-α)** – Drive acute inflammation via signaling pathways like NF-κB, not resolution.
**Clinical Pearl / High-Yield Fact**
SPMs like resolvins are