Inflammation and Repair — MCQs

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 51: Which of the following is an anti-inflammatory mediator?

A. Interleukin 4 (Correct Answer)
B. Interleukin 1
C. Interleukin 6
D. TNF-Alpha

Explanation: **Explanation:** Inflammation is a tightly regulated process balanced by pro-inflammatory and anti-inflammatory mediators [1]. The correct answer is **Interleukin-4 (IL-4)** because it primarily functions to downregulate the inflammatory response. **Why IL-4 is correct:** IL-4 is a key cytokine produced by Th2 cells. It acts as an anti-inflammatory mediator by inhibiting the production of pro-inflammatory cytokines (like IL-1, TNF-α, and IL-6) and suppressing the activity of M1 (pro-inflammatory) macrophages. Crucially, IL-4 promotes the **Alternative Activation of Macrophages (M2 pathway)**, which is essential for tissue repair, fibrosis, and the resolution of inflammation [3]. **Why the other options are incorrect:** * **Interleukin-1 (IL-1):** A potent pro-inflammatory cytokine produced by macrophages. It induces fever (endogenous pyrogen), increases the expression of adhesion molecules on endothelium, and activates neutrophils [1]. * **Interleukin-6 (IL-6):** A major pro-inflammatory cytokine that stimulates the liver to produce **Acute Phase Reactants** (like CRP and Fibrinogen). It also plays a role in inducing fever [1]. * **TNF-Alpha:** A "master regulator" of inflammation. It promotes leukocyte recruitment, stimulates cytokine cascades, and, in high concentrations, can lead to septic shock and cachexia [1]. **NEET-PG High-Yield Pearls:** * **Anti-inflammatory Mediators (The "Resolution" Team):** IL-10 (the most potent), IL-4, IL-13, and TGF-β. * **Pro-inflammatory Mediators:** IL-1, IL-6, TNF-α, and IFN-γ [2]. * **M1 vs. M2 Macrophages:** M1 is induced by IFN-γ (Microbicidal); M2 is induced by IL-4 and IL-13 (Repair/Anti-inflammatory) [3]. * **IL-8** is the most specific chemotactic agent for neutrophils. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 97-99. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106.

Question 52: Which of the following statements is NOT true about cytokines?

A. Cytokines are polypeptides.
B. Cytokines can exert autocrine and paracrine effects.
C. Cytokines are involved in leukocytic movements.
D. Cytokines participate in intrinsic enzymatic reactions. (Correct Answer)

Explanation: Cytokines are low-molecular-weight soluble proteins or **polypeptides** that act as mediators of inflammation and immune responses [1]. **Why Option D is the Correct Answer (The False Statement):** Cytokines do **not** possess intrinsic enzymatic activity. Unlike enzymes, they function by binding to specific high-affinity cell surface receptors. This binding triggers intracellular signaling cascades (most commonly the **JAK-STAT pathway**) to alter gene expression. They act as signaling molecules rather than catalysts for biochemical reactions. **Analysis of Other Options:** * **Option A:** Cytokines are indeed **polypeptides** produced by various cells, primarily activated lymphocytes, macrophages, and dendritic cells [1]. * **Option B:** They exhibit multiple modes of action: **Autocrine** (acting on the cell that secreted them), **Paracrine** (acting on adjacent cells), and occasionally **Endocrine** (systemic effects, e.g., IL-1 and TNF causing fever). * **Option C:** A specific subset of cytokines called **Chemokines** (e.g., IL-8) is responsible for stimulating leukocyte chemotaxis and controlling leukocyte movement from the blood into tissues [1]. **High-Yield NEET-PG Pearls:** * **TNF and IL-1:** The "master cytokines" of acute inflammation; they induce the expression of adhesion molecules (E-selectin) on endothelium. * **JAK-STAT Pathway:** The most common signaling pathway for cytokine receptors; mutations in this pathway are linked to myeloproliferative neoplasms. * **Pleiotropy:** The ability of one cytokine to act on multiple cell types (e.g., IL-4 acting on B-cells, T-cells, and mast cells). * **Redundancy:** Multiple cytokines exerting the same functional effect [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-99.

Question 53: Pain during inflammation is mediated by which of the following substances?

A. Nitric oxide
B. Leukotriene B4
C. Bradykinin (Correct Answer)
D. Chemokines

Explanation: ### Explanation **Correct Answer: C. Bradykinin** The cardinal signs of inflammation (Rubor, Calor, Tumor, Dolor, and Functio laesa) are mediated by specific chemical compounds. **Pain (Dolor)** is primarily mediated by **Bradykinin** and **Prostaglandins (specifically PGE2)** [1]. Bradykinin is a potent inflammatory mediator derived from the kinin system. It acts on B1 and B2 receptors to sensitize nociceptors (pain receptors) and cause direct stimulation of nerve endings [1]. While Prostaglandins do not cause pain directly, they lower the threshold for pain (hyperalgesia), making the effect of Bradykinin more intense [1]. --- ### Analysis of Incorrect Options: * **A. Nitric Oxide (NO):** Primarily responsible for **vasodilation** (Rubor and Calor) and has some bactericidal activity. It also helps in reducing the inflammatory response by inhibiting platelet aggregation [1]. * **B. Leukotriene B4 (LTB4):** This is a potent **chemotactic agent** [1]. Its primary role is the recruitment and activation of neutrophils to the site of injury. It does not directly mediate pain. * **C. Chemokines:** These are small proteins (like IL-8) that act as **chemoattractants** for specific types of white blood cells [1]. They guide the migration of cells but are not primary mediators of the pain response. --- ### NEET-PG High-Yield Pearls: * **Mediators of Pain:** Bradykinin and PGE2 [1]. * **Mediators of Fever:** IL-1, TNF, and PGE2 (acting on the hypothalamus) [1]. * **Mediators of Vasodilation:** Histamine, Prostaglandins, and Nitric Oxide [1]. * **Mediators of Increased Vascular Permeability:** Histamine, C3a, C5a, and Leukotrienes (LTC4, LTD4, LTE4) [1]. * **Chemotaxis "Big Four":** LTB4, C5a, IL-8, and Bacterial products (N-formyl methionine) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101.

Question 54: Which of the following is NOT a role of histamine in acute inflammation?

A. Mediates increase in vascular permeability
B. Mediates chemotaxis
C. Facilitates release of pain-causing substances
D. Causes vasoconstriction (Correct Answer)

Explanation: ### Explanation **1. Why Option D is the Correct Answer:** Histamine is a potent **vasodilator**, not a vasoconstrictor [1]. In the early stages of acute inflammation, histamine is released primarily by mast cell degranulation. It acts on **H1 receptors** located on vascular smooth muscle cells to cause **vasodilation** of arterioles, which increases blood flow (leading to redness and heat) [2]. Therefore, stating it causes vasoconstriction is physiologically incorrect in the context of inflammation. **2. Analysis of Incorrect Options:** * **Option A (Vascular Permeability):** This is the hallmark effect of histamine. It causes contraction of endothelial cells, creating **interendothelial gaps** in post-capillary venules [1]. This leads to protein-rich fluid leakage (exudate) and subsequent edema [3]. * **Option B (Chemotaxis):** While histamine is primarily known for vascular changes, it also acts as a minor chemoattractant, particularly for **eosinophils** (via H4 receptors), aiding in the recruitment of inflammatory cells to the site of injury. * **Option C (Pain):** Histamine indirectly facilitates pain by sensitizing nociceptors and stimulating the release of other mediators like prostaglandins and bradykinin [4], which are the primary mediators of the "Dolor" (pain) component of inflammation [1]. **3. NEET-PG High-Yield Pearls:** * **Source:** Mast cells (richest source), basophils, and platelets. * **Stimuli for Release:** IgE-mediated Type I Hypersensitivity, physical injury (cold/heat), and C3a/C5a (Anaphylatoxins). * **Site of Action:** Histamine-induced permeability occurs exclusively in the **post-capillary venules** [3]. * **Sequence of Events:** Histamine is the **first mediator** to be released during the "immediate transient response" (lasting 15–30 minutes) [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 84-85. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 187-188. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101.

Question 55: The epithelioid cell is a modified-

A. Macrophage (Correct Answer)
B. Lymphocyte
C. Mast cell
D. Eosinophil

Explanation: ### Explanation **Correct Answer: A. Macrophage** **Why it is correct:** Epithelioid cells are the hallmark of **granulomatous inflammation**. They are essentially **activated macrophages** that have undergone a morphological transformation [1]. Under the influence of cytokines (primarily **IFN-̳** produced by Th1 cells), macrophages increase their cytoplasmic volume and develop indistinct cell borders, causing them to pack closely together—resembling epithelial cells (hence the name "epithelioid") [1]. Unlike regular macrophages, epithelioid cells have reduced phagocytic activity but increased secretory capacity. **Why the other options are incorrect:** * **B. Lymphocyte:** While lymphocytes (specifically T-cells) are crucial in the formation of a granuloma by secreting the cytokines that activate macrophages, they do not transform into epithelioid cells [1]. * **C. Mast cell:** Mast cells are involved in Type I hypersensitivity and acute inflammation (releasing histamine). They are not precursors to epithelioid cells. * **D. Eosinophil:** Eosinophils are associated with parasitic infections and allergic reactions. While they may be present in certain granulomas (like Churg-Strauss syndrome), they do not form epithelioid cells. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Epithelioid cells have a pale pink granular cytoplasm and an oval, "slipper-shaped" or "footprint" nucleus [1]. * **Giant Cells:** When epithelioid cells fuse together, they form **Multinucleated Giant Cells** (e.g., Langhans giant cells in TB, where nuclei are arranged in a horseshoe pattern) [1]. * **Key Cytokine:** **Interferon-gamma (IFN-̳)** is the most important mediator for the transformation of macrophages into epithelioid cells [1]. * **Granuloma Definition:** A microscopic aggregation of epithelioid cells surrounded by a collar of lymphocytes and plasma cells [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-109.

Question 56: During internal injury, leukocytes are recruited by which of the following?

A. IL-1 (Correct Answer)
B. Selectin
C. Integrin
D. IL-6

Explanation: Leukocyte recruitment to the site of injury is a multi-step process regulated by cytokines and adhesion molecules. [1] **Why IL-1 is the correct answer:** **Interleukin-1 (IL-1)** and **TNF-̑** are the primary "pro-inflammatory cytokines" produced by macrophages and dendritic cells upon sensing injury or pathogens. Their critical role in recruitment is to **activate the vascular endothelium**. They induce the expression of adhesion molecules (E-selectin and ligands for integrins) on the endothelial surface, which allows circulating leukocytes to begin the process of rolling and firm adhesion. [1] Without IL-1/TNF-̑, the "signals" for recruitment would not be expressed on the vessel wall. **Why the other options are incorrect:** * **Selectins (Option B):** These are **adhesion molecules**, not recruitment signals. They mediate the initial "rolling" phase of leukocyte migration. [1] While necessary for the process, they are *expressed in response* to cytokines like IL-1. * **Integrins (Option C):** These are **surface proteins** found on leukocytes that mediate "firm adhesion" to the endothelium. [1] Like selectins, they are tools used in the process, not the initiating recruitment signals. * **IL-6 (Option D):** While IL-6 is a pro-inflammatory cytokine, its primary role is the **systemic acute-phase response** (e.g., inducing fever and stimulating the liver to produce CRP). It is not the primary driver of local leukocyte recruitment. [3] **NEET-PG High-Yield Pearls:** * **Sequence of Recruitment:** Margination → Rolling (Selectins) → Adhesion (Integrins) → Diapedesis (PECAM-1/CD31) → Chemotaxis (C5a, LTB4, IL-8). [1], [2] * **IL-1 & TNF:** The "Master Regulators" of endothelial activation. * **Chemokine for Neutrophils:** **IL-8** is the most potent chemoattractant specifically for neutrophils. * **Deficiency:** Leukocyte Adhesion Deficiency (LAD) type 1 is a defect in **Integrins (CD18)**, leading to delayed umbilical cord separation and lack of pus formation. [2] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 83-84.

Question 57: What are the most characteristic features of acute inflammation?

A. Vasoconstriction
B. Vascular stasis
C. Vasodilation and increased vascular permeability (Correct Answer)
D. Margination of leukocytes

Explanation: **Explanation:** Acute inflammation is the immediate and early response to injury, designed to deliver leukocytes and plasma proteins to the site of damage [1]. The process is defined by two major components: **vascular changes** and **cellular events** [1]. **Why Option C is Correct:** The hallmark of acute inflammation involves a shift in hemodynamics. **Vasodilation** (induced by mediators like histamine and nitric oxide) increases blood flow to the area, causing redness (rubor) and heat (calor) [2]. This is followed by **increased vascular permeability**, primarily in the post-capillary venules [3]. This "leakiness" allows protein-rich fluid (exudate) to move into the extravascular space, leading to edema (tumor) [1]. These two processes are the most fundamental and characteristic early changes that facilitate all subsequent inflammatory steps. **Analysis of Incorrect Options:** * **A. Vasoconstriction:** This is a transient, inconsistent reflex lasting only seconds. It is not a defining feature of the inflammatory process. * **B. Vascular Stasis:** While stasis occurs as a result of fluid loss and increased blood viscosity, it is a *consequence* of increased permeability rather than the primary characteristic feature. * **D. Margination of Leukocytes:** This is a crucial **cellular event**, but it occurs secondary to the vascular changes (stasis) [1]. Without the initial vasodilation and increased permeability, leukocytes would continue to flow in the central axial stream of the vessel. **NEET-PG High-Yield Pearls:** * **The "Gold Standard" Mechanism:** The most common mechanism of increased vascular permeability is **endothelial cell contraction**, leading to intercellular gaps in post-capillary venules [3]. * **Lewis Triple Response:** Includes flush (capillary dilatation), flare (arteriolar dilatation), and wheal (exudation/edema) [2]. * **Sequence of Events:** Vasodilation → Increased permeability → Stasis → Leukocyte Margination → Rolling → Adhesion → Transmigration (Diapedesis) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 83-85. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 187-188.

Question 58: What is the most important inflammatory mediator?

A. TNF (Correct Answer)
B. IL2
C. Interferon
D. PAF

Explanation: **Explanation:** **TNF (Tumor Necrosis Factor)** is considered the most important mediator in the acute inflammatory response, particularly in the context of systemic inflammation and the recruitment of leukocytes [1]. Produced primarily by activated macrophages and T-cells, TNF (along with IL-1) stimulates the expression of adhesion molecules (E-selectin and ligands for integrins) on endothelial cells, facilitating leukocyte rolling and adhesion [1]. It also stimulates the secretion of other cytokines and chemokines, making it a "master regulator" of the inflammatory cascade. **Why other options are incorrect:** * **IL-2:** This is primarily a T-cell growth factor. It is essential for the proliferation and differentiation of T-lymphocytes into effector and memory cells but is not a primary mediator of the general inflammatory response. * **Interferons (IFNs):** While IFN-γ is a potent activator of macrophages (chronic inflammation), interferons are primarily associated with antiviral responses and immune modulation rather than being the "most important" general inflammatory mediator. * **PAF (Platelet Activating Factor):** PAF causes platelet aggregation, vasodilation, and bronchoconstriction. While potent, its scope of action is narrower compared to the systemic and multi-level regulatory effects of TNF. **NEET-PG High-Yield Pearls:** * **Systemic Effects:** TNF and IL-1 are the primary mediators of the "Acute Phase Response," causing fever (via PGE2), lethargy, and hepatic synthesis of acute-phase proteins [1]. * **Septic Shock:** High concentrations of TNF are responsible for the clinical manifestations of septic shock, including hypotension, metabolic acidosis, and disseminated intravascular coagulation (DIC). * **Therapeutic Target:** TNF antagonists (e.g., Etanercept, Infliximab) are mainstay treatments for chronic inflammatory diseases like Rheumatoid Arthritis and IBD [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-101.

Question 59: Eosinophilia is typically found in infections caused by which of the following organisms?

A. Cryptococcus
B. Human Papillomavirus (HPV)
C. Strongyloides (Correct Answer)
D. Typhoid

Explanation: **Explanation:** **Correct Answer: C. Strongyloides** The hallmark of helminthic (parasitic) infections is **Eosinophilia** [1], [2]. When parasites like *Strongyloides stercoralis* invade tissues, they trigger a Type I and Type IV hypersensitivity reaction. The immune response is mediated by **Th2 cells**, which secrete **Interleukin-5 (IL-5)**. IL-5 is the potent chemoattractant responsible for the proliferation, activation, and recruitment of eosinophils. Eosinophils contain Major Basic Protein (MBP) in their granules, which is specifically designed to destroy the tough teguments of helminths. **Analysis of Incorrect Options:** * **A. Cryptococcus:** This is a fungus. Fungal infections typically elicit a **granulomatous inflammation** (chronic inflammation) characterized by macrophages and lymphocytes [2], not eosinophilia. * **B. Human Papillomavirus (HPV):** This is a viral infection. Viral infections generally result in **lymphocytosis** [2]. HPV specifically causes epithelial proliferation (koilocytic changes). * **D. Typhoid (*Salmonella typhi*):** Classically, Typhoid fever is associated with **Neutropenia and Eosinopenia** (disappearance of eosinophils). The presence of eosinophils often helps rule out active typhoid in a clinical setting [2]. **NEET-PG High-Yield Pearls:** * **NAACP** is a mnemonic for causes of Eosinophilia: **N**eoplasia, **A**llergy/Asthma, **A**ddison’s disease, **C**onnective tissue disorders, and **P**arasites [1]. * **Charcot-Leyden Crystals:** These are bipyramidal crystals found in sputum or stool, formed from the breakdown of eosinophil membranes (Galectin-10). * **Loeffler Syndrome:** Transient pulmonary eosinophilia occurring during the lung-migration phase of parasites like *Ascaris* or *Strongyloides*. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 592. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 195-196.

Question 60: In acute inflammation, pain is primarily mediated by which of the following substances?

A. Serotonin
B. Histamine
C. Bradykinin (Correct Answer)
D. Cytokines

Explanation: **Explanation:** In the process of acute inflammation, the cardinal sign of **Pain (Dolor)** is primarily mediated by **Bradykinin** and **Prostaglandins (PGE2)** [1]. **1. Why Bradykinin is correct:** Bradykinin is a potent inflammatory mediator derived from the kinin system (activated by Hageman factor/Factor XII). It acts directly on nociceptors (pain receptors) in the peripheral nervous system, increasing their sensitivity [1]. While Prostaglandins also cause pain, they primarily act by "sensitizing" the nerve endings to other mediators like Bradykinin [1]. Therefore, Bradykinin is considered the direct chemical mediator of the pain response. **2. Analysis of Incorrect Options:** * **A. Serotonin:** Primarily released by platelets; its main roles are vasoconstriction and acting as a neurotransmitter [1]. It does not play a primary role in the pain of acute inflammation. * **B. Histamine:** Released by mast cells, it is the chief mediator of **vasodilation** and **increased vascular permeability** (leading to redness and swelling/edema), but it does not directly mediate pain [1]. * **C. Cytokines:** While TNF and IL-1 are crucial for the systemic acute phase response (fever, leucocytosis), they do not directly stimulate pain receptors [1]. **3. NEET-PG High-Yield Pearls:** * **Mediators of Vasodilation:** Histamine and Nitric Oxide (NO). * **Mediators of Increased Permeability:** Histamine, Bradykinin, and Leukotrienes (C4, D4, E4) [1]. * **Mediators of Fever:** IL-1, TNF, and Prostaglandins (PGE2) [1]. * **Mediators of Chemotaxis:** C5a, LTB4, and IL-8 [1]. * **Pain Duo:** Remember **Bradykinin** (direct) and **PGE2** (sensitizer) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101.

Practice by Chapter

Acute Inflammation: Vascular Events

Practice Questions

Acute Inflammation: Cellular Events

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Chemical Mediators of Inflammation

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Chronic Inflammation

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Granulomatous Inflammation

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Systemic Effects of Inflammation

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Wound Healing

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Tissue Regeneration

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Fibrosis and Repair

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Resolution of Inflammation

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