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• W1993214296 abstract "Lyme disease is caused by the spirochete Borrelia burgdorferi and is transmitted through ticks. Inhibition of host skin’s innate immune response might be instrumental to both tick feeding and B. burgdorferi transmission. The article by Marchal et al. describes how tick saliva suppresses B. burgdorferi–induced antimicrobial peptide production. This inhibition directly facilitates survival of the spirochete and might lead to diminished chemotaxis of leukocytes toward the site of the tick bite. Lyme disease is caused by the spirochete Borrelia burgdorferi and is transmitted through ticks. Inhibition of host skin’s innate immune response might be instrumental to both tick feeding and B. burgdorferi transmission. The article by Marchal et al. describes how tick saliva suppresses B. burgdorferi–induced antimicrobial peptide production. This inhibition directly facilitates survival of the spirochete and might lead to diminished chemotaxis of leukocytes toward the site of the tick bite. Lyme disease, or Lyme borreliosis, was first recognized as a distinct clinical entity in 1975 in Old Lyme, Connecticut, in children at the Yale–New Haven Hospital who were initially thought to have juvenile rheumatoid arthritis (Steere et al., 1977Steere A.C. Malawista S.E. Snydman D.R. Shope R.E. Andiman W.A. Ross M.R. et al.Lyme arthritis: an epidemic of oligoarticular arthritis in children and adults in three Connecticut communities.Arthritis Rheum. 1977; 20: 7-17Crossref PubMed Scopus (877) Google Scholar). Previously, however, certain clinical signs of the disease had been described in Europe (Afzelius, 1921Afzelius A. Erythema chronicum migrans.Acta Derm Venereol. 1921; 2: 120-125Google Scholar). Ixodes scapularis, Ixodes ricinus, and Ixodes persulcatus are the most important vectors for Lyme borreliosis in the United States, Europe, and Asia, respectively, and the disease is caused by spirochetes of the Borrelia burgdorferi sensu lato group (Wang et al., 1999Wang G. van Dam A.P. Schwartz I. Dankert J. Molecular typing of Borrelia burgdorferi sensu lato: taxonomic, epidemiological, and clinical implications.Clin Microbiol Rev. 1999; 12: 633-653PubMed Google Scholar). In Europe and Asia, three major Borrelia genospecies (B. burgdorferi sensu stricto, Borrelia garinii, and Borrelia afzelii) are the causative agents. By contrast, only B. burgdorferi sensu stricto strains are present in the United States. The obligate enzootic life cycle of the spirochetes involves ticks, primarily Ixodes ticks, and a variety of vertebrate hosts, including small rodents, large mammals, and birds (Anderson and Magnarelli, 1980Anderson J.F. Magnarelli L.A. Vertebrate host relationships and distribution of ixodid ticks (Acari: Ixodidae) in Connecticut, USA.J Med Entomol. 1980; 17: 314-323Crossref PubMed Scopus (67) Google Scholar). In general, uninfected tick larvae acquire the bacterium by feeding on infected animals. Ticks remain infected during their consecutive molting periods, enabling both nymphal and adult ticks to transmit spirochetes to (larger) animals and humans. To secure attachment of the tick and to ensure susceptibility of reservoir hosts for future tick infestations, tick saliva contains modulators of host immune responses. During the course of a blood meal, which can take up to seven days, ticks introduce saliva containing a wide range of physiologically active components. Immunosuppressive proteins in tick saliva interfere with the host’s innate and adaptive immune responses (Figure 1), including inhibition of the complement cascade (Ribeiro, 1987Ribeiro J.M. Ixodes dammini: salivary anti-complement activity.Exp Parasitol. 1987; 64: 347-353Crossref PubMed Scopus (120) Google Scholar); binding of histamine (Mans, 2005Mans B.J. Tick histamine-binding proteins and related lipocalins: potential as therapeutic agents.Curr Opin Investig Drugs. 2005; 6: 1131-1135PubMed Google Scholar); impairment of natural killer cell (Kopecky and Kuthejlova, 1998Kopecky J. Kuthejlova M. Suppressive effect of Ixodes ricinus salivary gland extract on mechanisms of natural immunity in vitro.Parasite Immunol. 1998; 20: 169-174PubMed Google Scholar), dendritic cell (Hovius et al., 2008aHovius J.W. de Jong M.A. den Dunnen J. Litjens M. Fikrig E. van der Salp15 binding to DC-SIGN inhibits cytokine expression by impairing both nucleosome remodeling and mRNA stabilization.PLoS Pathog. 2008; 4: e31Crossref PubMed Scopus (144) Google Scholar), and neutrophil function (Montgomery et al., 2004Montgomery R.R. Lusitani D. de Boisfleury C.A. Malawista S.E. Tick saliva reduces adherence and area of human neutrophils.Infect Immun. 2004; 72: 2989-2994Crossref PubMed Scopus (66) Google Scholar); reduction in antibody titers (Wikel and Bergman, 1997Wikel S.K. Bergman D. Tick-host immunology: Significant advances and challenging opportunities.Parasitol Today. 1997; 13: 383-389Abstract Full Text PDF PubMed Scopus (97) Google Scholar); repression of production of cytokines such as interleukin (IL)-2, interferon-γ (Anguita et al., 2002Anguita J. Ramamoorthi N. Hovius J.W. Das S. Thomas V. Persinski R. et al.Salp15, an ixodes scapularis salivary protein, inhibits CD4(+) T cell activation.Immunity. 2002; 16: 849-859Abstract Full Text Full Text PDF PubMed Scopus (187) Google Scholar; Gillespie et al., 2001Gillespie R.D. Dolan M.C. Piesman J. Titus R.G. Identification of an IL-2 binding protein in the saliva of the Lyme disease vector tick, Ixodes scapularis.J Immunol. 2001; 166: 4319-4326Crossref PubMed Scopus (110) Google Scholar; Kotsyfakis et al., 2006Kotsyfakis M. Sa-Nunes A. Francischetti I.M. Mather T.N. Andersen J.F. Ribeiro J.M. Antiinflammatory and immunosuppressive activity of sialostatin L, a salivary cystatin from the tick Ixodes scapularis.J Biol Chem. 2006; 281: 26298-26307Crossref PubMed Scopus (155) Google Scholar), IL-4 (Muller-Doblies et al., 2007Muller-Doblies U.U. Maxwell S.S. Boppana V.D. Mihalyo M.A. McSorley S.J. Vella A.T. et al.Feeding by the tick, Ixodes scapularis, causes CD4(+) T cells responding to cognate antigen to develop the capacity to express IL-4.Parasite Immunol. 2007; 29: 485-499Crossref PubMed Scopus (19) Google Scholar), and IL-10 (Hannier et al., 2003Hannier S. Liversidge J. Sternberg J.M. Bowman A.S. Ixodes ricinus tick salivary gland extract inhibits IL-10 secretion and CD69 expression by mitogen-stimulated murine splenocytes and induces hyporesponsiveness in B lymphocytes.Parasite Immunol. 2003; 25: 27-37Crossref PubMed Scopus (48) Google Scholar); blocking of chemokine activity (Deruaz et al., 2008Deruaz M. Frauenschuh A. Alessandri A.L. Dias J.M. Coelho F.M. Russo R.C. et al.Ticks produce highly selective chemokine binding proteins with antiinflammatory activity.J Exp Med. 2008; 205: 2019-2031Crossref PubMed Scopus (155) Google Scholar); and inhibition of T-lymphocyte proliferation (Ramachandra and Wikel, 1992Ramachandra R.N. Wikel S.K. Modulation of host-immune responses by ticks (Acari: Ixodidae): effect of salivary gland extracts on host macrophages and lymphocyte cytokine production.J Med Entomol. 1992; 29: 818-826Crossref PubMed Scopus (150) Google Scholar). In recent years, many tick proteins with specific functions have been identified (reviewed by Hovius et al., 2008bHovius J.W. Levi M. Fikrig E. Salivating for knowledge: potential pharmacological agents in tick saliva.PLoS Med. 2008; 5: e43Crossref PubMed Scopus (89) Google Scholar). Importantly, immunosuppression by tick saliva may result in more efficient transmission of several tick-borne pathogens (Wikel, 1999Wikel S.K. Tick modulation of host immunity: an important factor in pathogen transmission.Int J Parasitol. 1999; 29: 851-859Crossref PubMed Scopus (197) Google Scholar).Tick salivary gland extract inhibits antimicrobial peptide production For both the tick and the spirochete, it is of paramount importance to inhibit the host innate immune response, the first line of host defense. A crucial part of the innate immune response against invading microorganisms is the complement cascade. Many bacteria, such as Streptococcus pneumoniae (Neeleman et al., 1999Neeleman C. Geelen S.P. Aerts P.C. Daha M.R. Mollnes T.E. Roord J.J. et al.Resistance to both complement activation and phagocytosis in type 3 pneumococci is mediated by the binding of complement regulatory protein factor H.Infect Immun. 1999; 67: 4517-4524Crossref PubMed Google Scholar) and Neisseria meningitidis (Ram et al., 1999Ram S. Mackinnon F.G. Gulati S. McQuillen D.P. Vogel U. Frosch M. et al.The contrasting mechanisms of serum resistance of Neisseria gonorrhoeae and group B Neisseria meningitidis.Mol Immunol. 1999; 36: 915-928Crossref PubMed Scopus (129) Google Scholar), have evolved mechanisms to inhibit complement-mediated killing. B. burgdorferi utilizes complement regulating–acquiring surface proteins (Kraiczy et al., 2001Kraiczy P. Skerka C. Kirschfink M. Zipfel P.F. Brade V. Mechanism of complement resistance of pathogenic Borrelia burgdorferi isolates.Int Immunopharmacol. 2001; 1: 393-401Crossref PubMed Scopus (101) Google Scholar) and Osp E/F related proteins (Alitalo et al., 2002Alitalo A. Meri T. Lankinen H. Seppala I. Lahdenne P. Hefty P.S. et al.Complement inhibitor factor H binding to Lyme disease spirochetes is mediated by inducible expression of multiple plasmid-encoded outer surface protein E paralogs.J Immunol. 2002; 169: 3847-3853Crossref PubMed Scopus (133) Google Scholar; Hellwage et al., 2001Hellwage J. Meri T. Heikkila T. Alitalo A. Panelius J. Lahdenne P. et al.The complement regulator factor H binds to the surface protein OspE of Borrelia burgdorferi.J Biol Chem. 2001; 276: 8427-8435Crossref PubMed Scopus (282) Google Scholar) to bind factor H or FHL protein and consequently inhibit complement-mediated borreliacidal activity. In addition, several tick salivary proteins have been identified that inhibit different pathways within the complement cascade (Schroeder et al., 2007Schroeder H. Daix V. Gillet L. Renauld J.C. Vanderplasschen A. The paralogous salivary anti-complement proteins IRAC I and IRAC II encoded by Ixodes ricinus ticks have broad and complementary inhibitory activities against the complement of different host species.Microbes Infect. 2007; 9: 247-250Crossref PubMed Scopus (38) Google Scholar; Schuijt et al., 2008Schuijt T.J. Hovius J.W. van Burgel N.D. Ramamoorthi N. Fikrig E. van Dam A.P. Salp15 inhibits the killing of serum sensitive Borrelia burgdorferi sensu lato isolates.Infect Immun. 2008; 76: 2888-2894Crossref PubMed Scopus (69) Google Scholar; Tyson et al., 2008Tyson K.R. Elkins C. de Silva A.M. A novel mechanism of complement inhibition unmasked by a tick salivary protein that binds to properdin.J Immunol. 2008; 180: 3964-3968Crossref PubMed Scopus (50) Google Scholar; Valenzuela et al., 2000Valenzuela J.G. Charlab R. Mather T.N. Ribeiro J.M. Purification, cloning, and expression of a novel salivary anticomplement protein from the tick, Ixodes scapularis.J Biol Chem. 2000; 275: 18717-18723Crossref PubMed Scopus (184) Google Scholar). Innate immune responses also include the family of antimicrobial peptides, an ancient form of host defense found in both plants and animals that possesses bactericidal capacities. Production of antimicrobial peptides at the site of infection—for instance, the skin—also results in chemotaxis of leukocytes. Marchal et al., 2009Marchal C.M.P. Luft B.J. Yang X. Sibilia J. Jaulhac B. Boulanger N.M. Defensin is suppressed by tick salivary gland extract during the in vitro interaction of resident skin cells with Borrelia burgdorferi..J Invest Dermatol. 2009; 129: 2515-2517Abstract Full Text Full Text PDF PubMed Scopus (30) Google Scholar and others demonstrate that B. burgdorferi is able to induce the production of several antimicrobial peptides, including human β-defensin-2 and cathelicidin LL-37, in human resident skin cells (fibroblasts and keratinocytes). In addition, they show that a selection of these antimicrobial peptides exhibit transient growth-inhibiting properties against B. burgdorferi. Induction of antimicrobial peptides could favor a robust innate immune response at the site of the tick bite, which could not only result in clearance of B. burgdorferi but also hamper tick feeding. Interestingly, Marchal and collaborators now demonstrate that salivary gland extract from Ixodes ricinus has the capacity to inhibit B. burgdorferi–induced antimicrobial peptide production. This would favor B. burgdorferi survival and facilitate infection as well as inhibit chemotaxis of leukocytes to the site of the tick bite, thereby making the tick–host–pathogen interface a less hostile environment and favoring tick attachment to the host. Identification of novel functions of tick saliva and tick salivary gland extract contributes to the understanding of the pathogenesis of Lyme disease. This may help researchers identify tick saliva proteins that could serve as templates for new pharmacological compounds and could reveal new ways to prevent or treat tick-borne infections such as Lyme disease and other emerging tick-borne infections." @default.
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• W1993214296 date "2009-10-01" @default.
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• W1993214296 title "Spitting Image: Tick Saliva Assists the Causative Agent of Lyme Disease in Evading Host Skin’s Innate Immune Response" @default.
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