The CD48 receptor mediates Staphylococcus aureus human and murine eosinophil activation

Abstract

These data demonstrate the important role of CD48 in SA/exotoxins-eosinophil activating interactions that can take place during allergic responses and indicate CD48 as a novel therapeutic target for allergy and especially of AD.

Staphylococcus aureus and primary lysis of eosinophils

“…As evidenced by electron microscopy analysis, the occurrence of primary lysis may dominate the diseased tissue scene with more than 80% of eosinophils exhibiting cytolysis (reviewed in 3). Importantly, this ultimate mode of eosinophil activation agrees with in vivo observations in human diseased tissues in asthma and atopic dermatitis, the two conditions discussed by Minai-Fleminger et al [1]. In turn, the FEGs release their toxic proteins and cytokines [2,3].…”

“…I read with interest the comprehensive report by Minai-Fleminger et al [1] on eosinophil activation by Staphylococcus aureus (S. aureus). The authors focus on possible involvement of CD48 in eosinophil activation and forward the possibility that blocking CD48 is of therapeutic interest.…”

Roles of CD48 in regulating immunity and tolerance

“…Furthermore, eosinophils from CD48−/− [B6.129] mice do not perform these functions as well as WT eosinophils. In a model of peritonitis induced by intraperitoneal injection of Staphylococcal toxin B (SEB), CD48−/− [B6.129] mice had reduced numbers of eosinophils and granulocytes in peritoneal lavage fluid, but no reduction in lymphocytes, when compared to WT mice [116]. These studies indicate that CD48 can contribute to bacterial sensing and granulocyte activation during infection.…”

Author response to ‘Staphylococcus aureus and primary lysis of eosinophils’ by Dr Persson

“…However, in our experimental settings (using heatinactivated SA), although EETs were observed, no eosinophil cytolysis was detected (as examined by morphology, viability staining and cell counting) [1]. Interestingly, the presence of blocking anti-CD48 antibodies enhanced EET release without causing cell death.…”

“…Nevertheless, our current studies [1] focus on the role of CD48 in eosinophil activation and did not address the EET mechanism. Therefore, nor the source of DNA or the existence of FEGs or granule proteins in the EETs were examined in our SA-eosinophil co-cultures.…”