A Novel Role for CD55 in Granulocyte Homeostasis and Anti-Bacterial Host Defense

نویسندگان

  • Henrike Veninga
  • Robert M. Hoek
  • Alex F. de Vos
  • Alex M. de Bruin
  • Feng-Qi An
  • Tom van der Poll
  • René A. W. van Lier
  • M. Edward Medof
  • Jörg Hamann
چکیده

BACKGROUND In addition to its complement-regulating activity, CD55 is a ligand of the adhesion class G protein-coupled receptor CD97; however, the relevance of this interaction has remained elusive. We previously showed that mice lacking a functional CD97 gene have increased numbers of granulocytes. METHODOLOGY/RESULTS Here, we demonstrate that CD55-deficient mice display a comparable phenotype with about two-fold more circulating granulocytes in the blood stream, the marginated pool, and the spleen. This granulocytosis was independent of increased complement activity. Augmented numbers of Gr-1-positive cells in cell cycle in the bone marrow indicated a higher granulopoietic activity in mice lacking either CD55 or CD97. Concomitant with the increase in blood granulocyte numbers, Cd55⁻/⁻ mice challenged with the respiratory pathogen Streptococcus pneumoniae developed less bacteremia and died later after infection. CONCLUSIONS Collectively, these data suggest that complement-independent interaction of CD55 with CD97 is functionally relevant and involved in granulocyte homeostasis and host defense.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Transcript analysis of some defense genes of tomato in response to host and non-host bacterial pathogens

The transcript levels of six defense genes including pathogenesis-related gene 1 (PR-1), pathogenesis-related gene 2 (PR-2), pathogenesis-related gene 5 (PR-5), lipoxygenase (LOX), phenylalanine ammonia-lyase (PAL) and catalase (CAT) were investigated in tomato plants inoculated with Xanthomonas axonopodis pv. phaseoli as a non-host pathogen and X. euvesicatoria as a host pathogen. Activation o...

متن کامل

Therapeutic Administration of a Monoclonal Anti-Il-1β Antibody Protects Against Experimental Melioidosis

BACKGROUND Melioidosis, caused by the gram-negative bacterium Burkholderia pseudomallei, is a common cause of community-acquired sepsis in Southeast Asia and Northern Australia. The NLRP3 inflammasome and its downstream product interleukin-1 beta (IL-1β) have been proposed to play crucial roles in melioidosis. In this study, we characterized the role of IL-1β more closely and we assessed its th...

متن کامل

پیشگیری از آنتروکولیت نکروزان

  NEC (Necrotizing Enterocolitis) is an increasing clinical burden to patients, families, and the neonatology health care team. Although the diagnosis is straightforward, the morbidity and mortality associated with the disease are not improving. Risk factors of prematurity, formula feeding, intestinal ischemia/hypoxia, and bacterial colonization accentuate the imbalance toward mucosal stress wi...

متن کامل

بررسی حضور ماست‌سل‌ها درپریودنتیت مهاجم

Background and Objective: Aggressive periodontitis is a destructive disease that leads to a quick and extensive periodontal tissue loss. Mast cells are known to play important roles in allergic reactions, host defense against bacterial infections, local homeostasis, inflammation, and angiogenesis. The aim of the present study was to evaluate the relationship between mast cell numbers and aggres...

متن کامل

Epigenetic Modifications of Host Genes Induced by Bacterial Infection

Introduction: Epigenetic mechanisms regulate expression of the genome to generate various cell types during development or coordinate cellular responses to external stimulus. While epigenetics is of fundamental importance in eukaryotes, it plays a different role in bacteria. This article uncovers the most important recent data on how bacteria can alter epigenetic marks and can also contribute t...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره 6  شماره 

صفحات  -

تاریخ انتشار 2011