Close Association between Pulmonary Disease Manifestation inMycoplasma pneumoniaeInfection and Enhanced Local Production of Interleukin-18 in the Lung, Independent of Gamma Interferon

Abstract

To investigate pathophysiologies of

Significant Role of Interleukin-8 in Pathogenesis of Pulmonary Disease Due to Mycoplasma pneumoniae Infection

“…On the other hand, the results for IL-8 obtained in this study strongly suggest that this cytokine, specifically produced in the lung, plays a significant role in the pathomechanism of a sustained fibrotic change of the lung which we suspect to be a consequence of intraluminal organization (5). It has been widely recognized that the pathologic feature of M. pneumoniae pneumonia is characterized by the mononuclear cell or lymphoplasmacytic cell infiltration at the site of inflammation (1,2,7,9).…”

“…More recently, it was reported that interleukin-18 (IL-18), a regulatory cytokine for Th1-type cytokines, plays an important role in pulmonary disease manifestation due to M. pneumoniae (5). In that study, significantly elevated levels of IL-18 were found in pleural fluid (PF) samples from patients with massive pleural effusion and with a sustained fibrotic change of the lung on chest roentgenograms, presumably as a result of combination of mainly intraluminal organization (10) and, to a lesser extent, pulmonary fibrosis.…”

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].…”

Multiple Hepatic Receptors Cooperate to Eliminate Secretory Mucins Aberrantly Entering the Bloodstream: Are Circulating Cancer Mucins the “Tip of the Iceberg”?

“…For example, the CA19-9 antibody detects sialyl Lewis A (Neu5Aca2-3Galh1-3[Fuca1-4]GlcNAc) presented on a circulating high-molecular-weight mucin, providing an assay for diagnosis and monitoring of stomach, colon, and pancreatic cancer (25); and O-glycans on circulating MUC16 recognized by antibody CA-125 provides for diagnosis and monitoring of ovarian cancers (26). ''False-positives'' in such assays arise in acute and chronic pancreatitis (27)(28)(29), acute cholangitis (30), cystic fibrosis (31), bacterial pneumonia (32), endometriosis (33), benign ovarian cysts, the first trimester of pregnancy, and pelvic inflammatory disease (33)(34)(35)(36). Thus, although such biomarker assays have focused on cancer detection, epithelial mucins can also apparently ''spill'' into the circulation in a broad range of pathologies involving hollow organs and/or glands, including injury or inflammation.…”