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      Perivascular macrophages mediate neutrophil recruitment during bacterial skin infection.

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          Abstract

          Transendothelial migration of neutrophils in postcapillary venules is a key event in the inflammatory response against pathogens and tissue damage. The precise regulation of this process is incompletely understood. We report that perivascular macrophages are critical for neutrophil migration into skin infected with the pathogen Staphylococcus aureus. Using multiphoton intravital microscopy we showed that neutrophils extravasate from inflamed dermal venules in close proximity to perivascular macrophages, which are a major source of neutrophil chemoattractants. The virulence factor α-hemolysin produced by S. aureus lyses perivascular macrophages, which leads to decreased neutrophil transmigration. Our data illustrate a previously unrecognized role for perivascular macrophages in neutrophil recruitment to inflamed skin and indicate that S. aureus uses hemolysin-dependent killing of these cells as an immune evasion strategy.

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          Community-associated methicillin-resistant Staphylococcus aureus: epidemiology and clinical consequences of an emerging epidemic.

          Michael David, Robert S Daum (2010)
          Staphylococcus aureus is an important cause of skin and soft-tissue infections (SSTIs), endovascular infections, pneumonia, septic arthritis, endocarditis, osteomyelitis, foreign-body infections, and sepsis. Methicillin-resistant S. aureus (MRSA) isolates were once confined largely to hospitals, other health care environments, and patients frequenting these facilities. Since the mid-1990s, however, there has been an explosion in the number of MRSA infections reported in populations lacking risk factors for exposure to the health care system. This increase in the incidence of MRSA infection has been associated with the recognition of new MRSA clones known as community-associated MRSA (CA-MRSA). CA-MRSA strains differ from the older, health care-associated MRSA strains; they infect a different group of patients, they cause different clinical syndromes, they differ in antimicrobial susceptibility patterns, they spread rapidly among healthy people in the community, and they frequently cause infections in health care environments as well. This review details what is known about the epidemiology of CA-MRSA strains and the clinical spectrum of infectious syndromes associated with them that ranges from a commensal state to severe, overwhelming infection. It also addresses the therapy of these infections and strategies for their prevention.
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            Perivascular microglial cells of the CNS are bone marrow-derived and present antigen in vivo.

            W F Hickey, H. Kimura (1988)
            A crucial question in the study of immunological reactions in the central nervous system (CNS) concerns the identity of the parenchymal cells that function as the antigen-presenting cells in that organ. Rat bone marrow chimeras and encephalitogenic, major histocompatability--restricted T-helper lymphocytes were used to show that a subset of endogenous CNS cells, commonly termed "perivascular microglial cells," is bone marrow-derived. In addition, these perivascular cells are fully competent to present antigen to lymphocytes in an appropriately restricted manner. These findings are important for bone marrow transplantation and for neuroimmunological diseases such as multiple sclerosis.
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              Cutaneous immunosurveillance and regulation of inflammation by group 2 innate lymphoid cells.

              Ben Roediger, S. H. Kim, Graham Le Gros … (2013)
              Type 2 immunity is critical for defense against cutaneous infections but also underlies the development of allergic skin diseases. We report the identification in normal mouse dermis of an abundant, phenotypically unique group 2 innate lymphoid cell (ILC2) subset that depended on interleukin 7 (IL-7) and constitutively produced IL-13. Intravital multiphoton microscopy showed that dermal ILC2 cells specifically interacted with mast cells, whose function was suppressed by IL-13. Treatment of mice deficient in recombination-activating gene 1 (Rag1(-/-)) with IL-2 resulted in the population expansion of activated, IL-5-producing dermal ILC2 cells, which led to spontaneous dermatitis characterized by eosinophil infiltrates and activated mast cells. Our data show that ILC2 cells have both pro- and anti-inflammatory properties and identify a previously unknown interactive pathway between two innate populations of cells of the immune system linked to type 2 immunity and allergic diseases.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Nat. Immunol.
                Title: Nature immunology
                Publisher: Springer Nature
                ISSN (Electronic): 1529-2916
                ISSN (Print): 1529-2908
                Publication date (Electronic): Jan 2014
                Volume: 15
                Issue: 1
                Affiliations
                [1 ] 1] The Centenary Institute, Newtown, New South Wales, Australia. [2].
                [2 ] The Centenary Institute, Newtown, New South Wales, Australia.
                [3 ] School of Biological Sciences, University of Sydney, New South Wales, Australia.
                [4 ] Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia.
                [5 ] Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Biopolis, Singapore.
                [6 ] 1] The Centenary Institute, Newtown, New South Wales, Australia. [2] Sydney Medical School, New South Wales, Australia.
                [7 ] Immune Disease Institute and Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, USA.
                [8 ] 1] The Centenary Institute, Newtown, New South Wales, Australia. [2] Discipline of Dermatology, Sydney Medical School, New South Wales, Australia. [3] Department of Dermatology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia.
                Article
                Publisher Item ID: ni.2769 Mid ID: NIHMS577484
                DOI: 10.1038/ni.2769
                PMC ID: 4097073
                PubMed ID: 24270515
                SO-VID: 11e0616e-a4c1-4ba2-aebe-621e5bf32e13
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