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Acute Inflammation I: Inflammatory Response01:26

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Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect...
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The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...
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Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
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Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
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The plexin C1 receptor promotes acute inflammation.

Klemens König1, Linda Marth, Jan Roissant

  • 1Department of Anaesthesiology and Intensive Care Medicine, Tübingen University Hospital, Eberhard-Karls University Tübingen, Tübingen, Germany; Clinic of Anaesthesiology, Intensive Care Medicine and Pain Therapy, University Hospital Frankfurt am Main, Frankfurt, Germany.

European Journal of Immunology
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PubMed
Summary

Plexin C1 (PLXNC1) plays a key role in acute inflammation by influencing leukocyte behavior. Blocking PLXNC1 reduces inflammatory responses, suggesting it as a therapeutic target for inflammatory diseases.

Keywords:
InflammationNeuronal Guidance ProteinPlexin C1Semaphorin 7a

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Area of Science:

  • Immunology
  • Neuroscience
  • Molecular Biology

Background:

  • Acute inflammation underlies organ failure and is primarily regulated by chemokines.
  • Neuronal guidance cues, like semaphorin 7a, are increasingly recognized for their role in inflammation.
  • The function of plexin C1 (PLXNC1), a semaphorin 7a receptor, in inflammation remains largely unknown.

Purpose of the Study:

  • To investigate the role of plexin C1 (PLXNC1) in acute inflammatory responses.
  • To determine if PLXNC1 is a potential therapeutic target for inflammatory conditions.

Main Methods:

  • Utilized PLXNC1 knockout mice (PLXNC1-/-) and wild-type (WT) mice in a zymosan A (ZyA)-induced peritonitis model.
  • Assessed leukocyte rolling, adhesion, and transmigration in vivo and in vitro.
  • Employed chimeric mice to investigate the role of hematopoietic PLXNC1.
  • Administered anti-PLXNC1 antibody and a PLXNC1-binding peptide to WT mice to evaluate therapeutic potential.

Main Results:

  • PLXNC1 is expressed outside the nervous system and upregulated during acute inflammation.
  • PLXNC1 knockout mice exhibited significantly reduced inflammatory responses and altered leukocyte migration.
  • Blocking PLXNC1 in vitro attenuated transendothelial migration.
  • Hematopoietic deficiency of PLXNC1 led to attenuated inflammation.
  • Therapeutic blockade with anti-PLXNC1 antibody or peptide significantly reduced peritonitis in WT mice.

Conclusions:

  • Plexin C1 (PLXNC1) is critically involved in orchestrating acute inflammatory responses.
  • PLXNC1 influences leukocyte trafficking during inflammation.
  • PLXNC1 represents a promising therapeutic target for managing acute inflammatory diseases.