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Related Concept Videos

Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

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...
Myocarditis I: Introduction01:21

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Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
Myocarditis II: Clinical Features and Diagnostic Tests01:27

Myocarditis II: Clinical Features and Diagnostic Tests

Myocarditis is an inflammation of the heart muscle. The symptoms vary widely, encompassing asymptomatic presentations to severe, acute manifestations.Clinical PresentationAsymptomatic cases: In some instances, myocarditis may be asymptomatic, with the infection resolving without intervention. These cases often go undetected unless discovered incidentally through diagnostic imaging or tests conducted for other reasons.General Early Symptoms: Early symptoms of myocarditis are non-specific and can...
Inflammation01:38

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Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

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...
Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

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 damage-associated...

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Related Experiment Video

Updated: May 30, 2026

Human In-Vivo Bioassay for the Tissue-Specific Measurement of Nociceptive and Inflammatory Mediators
08:54

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Published on: December 1, 2008

Alexithymia and tissue inflammation.

Kirsi Honkalampi1, Soili M Lehto, Heli Koivumaa-Honkanen

  • 1Kuopio Psychiatric Center, Kuopio, Finland. kirsi.honkalampi @ kuh.fi

Psychotherapy and Psychosomatics
|August 11, 2011
PubMed
Summary

Inflammation marker high-sensitivity C-reactive protein (hs-CRP) is linked to alexithymia, a condition affecting emotional processing. This association is independent of depressive symptoms, suggesting a broader role for inflammation in stress-related conditions.

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Area of Science:

  • Psychoneuroimmunology
  • Clinical Psychology
  • General Population Health

Background:

  • Altered immune responses are implicated in depression.
  • Emerging evidence suggests similar immune changes may occur in alexithymia.
  • The relationship between inflammatory markers and alexithymia requires further investigation.

Purpose of the Study:

  • To investigate the independent association between inflammatory markers (hs-CRP and IL-6) and alexithymia in a general population sample.
  • To determine if these inflammatory markers are related to alexithymia or its specific factors.
  • To explore the interplay between inflammation, alexithymia, and depressive symptoms.

Main Methods:

  • Utilized data from the Kuopio Depression (KUDEP) general population study (n=308, adults aged 25-64).
  • Assessed alexithymia using the Toronto Alexithymia Scale (TAS-20).
  • Measured depressive symptoms with the Beck Depression Inventory (BDI-21) and inflammatory markers (hs-CRP, IL-6).

Main Results:

  • Significantly higher levels of IL-6 and hs-CRP were observed in individuals with alexithymia compared to non-alexithymic individuals.
  • High-sensitivity C-reactive protein (hs-CRP), but not IL-6, independently increased the likelihood of belonging to the alexithymic group.
  • Inflammatory markers and depressive symptoms explained 33.5% of the variance in alexithymia scores.

Conclusions:

  • The association between hs-CRP and alexithymia is comparable to that seen in depressed patients.
  • This hs-CRP-alexithymia link is independent of the presence of depressive symptoms.
  • Findings expand the understanding of the stress-alexithymia concept, highlighting a potential role for inflammation.