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Item Anthrax Lethal Toxin Impairs CD1d-Mediated Antigen Presentation by Targeting the Extracellular Signal-Related Kinase 1/2 Mitogen-Activated Protein Kinase Pathway(American Society for Microbiology, 2010-05) Khan, Masood A.; Gallo, Richard M.; Brutkiewicz, Randy R.; Microbiology and Immunology, School of MedicineLethal toxin (LT) is a critical virulence factor of Bacillus anthracis and an important means by which this bacterium evades the host's immune system. In this study, we demonstrate that CD1d-expressing cells treated with LT have reduced CD1d-mediated antigen presentation. We earlier showed an important role for the mitogen-activated protein kinase extracellular signal-regulated kinase 1/2 (ERK1/2) in the regulation of CD1d-mediated antigen presentation, and we report here that LT impairs antigen presentation by CD1d in an ERK1/2-dependent manner. Similarly, LT and the ERK1/2 pathway-specific inhibitor U0126 caused a decrease in major histocompatibility complex (MHC) class II-mediated antigen presentation. Confocal microscopy analyses revealed altered intracellular distribution of CD1d and LAMP-1 in LT-treated cells, similar to the case for ERK1/2-inhibited cells. These results suggest that Bacillus anthracis has the ability to evade the host's innate immune system by reducing CD1d-mediated antigen presentation through targeting the ERK1/2 pathway.Item Outer surface protein OspC is an antiphagocytic factor that protects Borrelia burgdorferi from phagocytosis by macrophages(American Society for Microbiology, 2015-12) Carrasco, Sebastian E.; Troxell, Bryan; Yang, Youyun; Brandt, Stephanie L.; Li, Hongxia; Sandusky, George E.; Condon, Keith W.; Serezani, C. Henrique; Yang, X. Frank; Department of Microbiology & Immunology, IU School of MedicineOuter surface protein C (OspC) is one of the major lipoproteins expressed on the surface of Borrelia burgdorferi during tick feeding and the early phase of mammalian infection. OspC is required for B. burgdorferi to establish infection in both immunocompetent and SCID mice and has been proposed to facilitate evasion of innate immune defenses. However, the exact biological function of OspC remains elusive. In this study, we showed that the ospC-deficient spirochete could not establish infection in NOD-scid IL2rγ(null) mice that lack B cells, T cells, NK cells, and lytic complement. The ospC mutant also could not establish infection in anti-Ly6G-treated SCID and C3H/HeN mice (depletion of neutrophils). However, depletion of mononuclear phagocytes at the skin site of inoculation in SCID and C3H/HeN mice allowed the ospC mutant to establish infection in vivo. In phagocyte-depleted mice, the ospC mutant was able to colonize the joints and triggered neutrophilia during dissemination. Furthermore, we found that phagocytosis of green fluorescent protein (GFP)-expressing ospC mutant spirochetes by murine peritoneal macrophages and human THP-1 macrophage-like cells, but not in PMN-HL60, was significantly higher than parental wild-type B. burgdorferi strains, suggesting that OspC has an antiphagocytic property. In addition, overproduction of OspC in spirochetes also decreased the uptake of spirochetes by murine peritoneal macrophages. Together, our findings provide evidence that mononuclear phagocytes play a key role in clearance of the ospC mutant and that OspC promotes spirochetes' evasion of macrophages during early Lyme borreliosis.Item Studies on the organization and regulation of the colonization factor antigen 1 (CFA/1) fimbrial system of escherichia coli(1990) Karjalainen, Tuomo KalleItem The Effect of Bonded Orthodontic Appliances on Salivary Mutans Streptococci and on Immunoglobulin A Antibody to S. Mutans(1997) Wittler, Michelle L.; Gregory, Richard L.; Switalski, Lech M.; Miller, Chris H.; Garetto, Lawrence P.; Shanks, James C.The placement of fixed orthodontic appliances creates a number of new retention sites in the oral cavity, which subsequently leads to an increase in the number of cariogenic bacteria, including Streptococcus mutans, during active orthodontic treatment. We hypothesize that the increased prevalence of S. mutans in the saliva of orthodontic patients provides an antigenic challenge to the mucosal immune system, which leads to an elevation of secretory IgA (sIgA) antibodies to S. mutans in saliva. The purpose of this study was to evaluate the change in numbers of salivary mutans streptococci and the concentration of parotid sIgA antibody to S. mutans with the placement of bonded orthodontic appliances. A randomly selected group of 19 patients requiring the placement of orthodontic appliances was tested in this study. Whole and parotid saliva samples were collected three times prior to bonding and four times during bonded appliance therapy over a 30-week period. Whole saliva samples were spiral plated on mitis salivarius sucrose agar and mitis salivarius sucrose bacitracin agar in order to quantify total oral streptococci and mutans streptococci, respectively. Parotid saliva was assayed for IgA antibody to S. mutans using an established ELISA technique. The results demonstrated a significant (p < 0.05) increase in total oral streptococci and mutans streptococci numbers after six months of orthodontic treatment when compared with the baseline values. The level of sIgA to the clinical isolates of S. mutans was also significantly higher six months after the cementation of orthodontic appliances. These elevated numbers of mutans streptococci elicited a mucosa! immune response, which corresponded with a higher concentration of sIgA to S. mutans in the saliva. There was a significant negative correlation (R = -0.22; p = 0.02) between the numbers of mutans streptococci and sIgA antibody levels to the clinical isolates of S. mutans. When the sIgA antibody levels were elevated the numbers of mutans streptococci were lower. These data suggest that sIgA antibody to S. mutans may be a protective mechanism against an elevated level of mutans streptococci caused by the placement of orthodontic appliances. If the mucosal immune response to S. mutans could be enhanced before bonding orthodontic appliances, this could prevent some of the demineralization found adjacent to bands and brackets.