Role of Interleukin-18 and T-helper Type 1 Cytokines in the Development of Mycoplasma pneumoniae Pneumonia in Adults

Clinical features, risk factors and treatment of fulminant Mycoplasma pneumoniae pneumonia: A review of the Japanese literature

“…Correlation of the radiological findings and severity of inflammation using inflammation markers indicated that mixed pattern cases had higher CRP (n = 5, 28.7 mg/dL) compared to that of interstitial (n = 26, 17.2 mg/dL) or alveolar pattern (n = 10, 19.1 mg/dL) cases, however, there was no statistical different (p = 0.143). No such trend was identified 10 when comparing the findings of WBC counts and ESR, either.…”

“…Varied chest radiographic patterns were recognized in patients with fulminant MPP, and these findings may reflect the difference in the immunological response (e.g., difference in cytokine production) [10]. Liver dysfunction such as ALT and AST elevation were common in fulminant MPP.…”

“…MPP is sometimes a self-limiting disease; however, the following are considered virulence-associated factors of MP: 1) direct interaction between human host cells caused by toxicity (e.g., adherence to bronchoepithelial cells, toxin production, reactive oxygen species, and cytokines), and 2) indirect interaction of immunological or allergic reaction to MP infection [9,10]. Although the apparent mechanism and etiology of fulminant MPP have not been revealed, there are at least 3 possible hypotheses: 1) hyperimmune response originating in the lung due to repeated childhood MP infections, 13 2) loss of the ability to eradicate MP from the lung in primary infection resulting in longer-lasting MP infection in the lung, which may cause a hyperimmune response, and 3) overactive innate immune response such as macrophage activation via heterodimerization of Toll-like receptors 2 and 6 of the bronchoepithelial cells to MP lipoproteins [11].…”

Mycoplasma pneumoniae as an Under- Recognized Agent of Vasculitic Disorders

“…Mycoplasma pneumoniae infection then leads to pneumonia by inducing various kinds of cytokines. Among a number of cytokines reported to be associated with the pathomechanism of M. pneumoniae pneumonia, the author and coworkers have demonstrated that the macrophage-derived cytokines interleukin-18 and interleukin-8 play significant roles in the development of pneumonia and are directly related to disease severity [Narita et al, 2000[Narita et al, , 2001aTanaka et al, 2002]. Interleukin-18 is an immune regulatory cytokine that functions as an activator of T cells and a subsequent cascade of T helper-1 and T helper-2 type cytokines [Tanaka et al, 1996].…”

Acute respiratory distress syndrome caused by Mycoplasma pneumoniae without elevated pulmonary vascular permeability: a case report

“…After M. pneumoniae infection, alveolar macrophages and T cells synergistically induce the cellular immune response by the release of proinflammatory cytokines leading to ARDS in individuals with hyperresponsiveness (13)(14)(15). Although open lung biopsy in ARDS is impracticable, autopsy cases of MPP with fatal respiratory failure have shown that mycoplasma organisms localized on the surface of bronchiolar epithelium, whereas the tissue inflammation and damage extended into deeper parts of the lungs (16), suggesting host immune responses to highly immunogenic molecules associated with M. pneumoniae.…”