scholarly journals Identification of Staphylococcus aureaus Virulence Factors Associated with Bovine Mastitis

2001 ◽  
Author(s):  
Lorraine Sordillo ◽  
Don Wojchowski ◽  
Gary Perdew ◽  
Arthur Saran ◽  
Gabriel Leitner
Keyword(s):  
Virulence Factors ◽  
Host Defense ◽  
Defense Mechanisms ◽  
Differentially Express ◽  
Cell Activity ◽  
Bovine Mastitis ◽  
Growth Potential ◽  
Differentially Expressed ◽  
Antigenic Determinants

Staphylococcus aureus is a major cause of mastitis in dairy cattle. The organism is able to adhere to and penetrate mammary epithelium, forming deep seated abscesses that result in chronic infections. This study was based on the observation that certain genotypes of S. aureus are isolated more frequently from field cases of bovine mastitis than others and the most prevalent genotypes of S. aureus have an increased ability to resist neutrophil phagocytosis and killing compared to the rare variants. It was hypothesized that these predominating genotypes differentially express virulence factors that allow them to overcome or suppress essential host defense mechanisms and successfully colonize mammary parenchyma. The overall objective of this study was to determine the mechanisms by which predominating S. aureus genotypes were able to resist mammary gland defense mechanisms. The following specific aims were accomplished to address the overall objectives of this project: 1. Analyze and compare cell surface and secreted protein profiles of common and rare S. aureus genotypes isolated from field cases of bovine mastitis. 2. Purify and sequence selectively synthesized proteins unique to the most prevalent genotypes of S. aureus . 3. Determine the in vitro effects of isolated proteins on essential host defense mechanisms. Results from each specific aim showed that these redominating genotypes differentially express factors that may allow them to overcome or suppress essential host defense mechanisms and successfully colonize mammary parenchyma. Using complementary approaches, both the US and Israeli teams identified differentially expressed S. aureus factors that were positively correlated with virulence as determined by the ability to modify host immune cell responses and increase disease pathogenesis. Several candidate virulence factors have ben identified at both the molecular (US team) and protein (Israeli team) levels. Components of the phosphotransferase system were shown to be differentially expressed in prevalent strains of S. aureus and to modify the growth potential of these strains in a milk microenvironment. Evidence provided by both the Israeli and US teams also demonstrated a potential role of Staphylococcal enterotoxins in the pathogenesis of mastitis. Certain enterotoxins were shown to directly affect neutrophil bactericidal activities which can profoundly affect the establishment of new intramammary infections. Other evidence suggests that S. aureus superantigens can suppress mammary defenses by enhancing lymphoid suppressor cell activity. Collectively, these data suggest that unique factors are associated with predominating S. aureus genotypes that can affect in vitro and in vivo virulence as related to the pathogenesis of bovine mastitis. The potential development of a subunit mastitis vaccine which incorporates only relevant antigenic determinants has not been investigated in depth. Experiments outlined in this proposal has identified putative virulence factors which contribute to the pathogenesis of S. aureus mastitis and which may be used to formulate an efficacious subunit mastitis vaccine. Results from these studies may lead to the development of new methods to prevent this costly disease, providing a viable alternative to less effective mastitis control procedures based on chemotherapy.

Neutrophil Adhesion Molecule Expression Is Comparable in Perinatal Rabbits and Humans

1997 ◽  
Vol 86 (2) ◽  
pp. 420-427 ◽  
Author(s):  
Chandra Ramamoorthy ◽  
Daniel W. Kovarik ◽  
Robert K. Winn ◽  
John M. Harlan ◽  
Sam R. Sharar
Keyword(s):  
Host Defense ◽  
Adhesion Molecule ◽  
Defense Mechanisms ◽  
Bacterial Infections ◽  
Perinatal Period ◽  
Surface Expression ◽  
Full Term ◽  
Fluorescence Labeling ◽  
Adhesion Molecule Expression

Background Human newborns, particularly those born before full term, are more susceptible to bacterial infections as a result of impaired host defense mechanisms. Compared with adults, circulating leukocytes from human newborns (preterm and full-term gestations) and newborn rabbits (full-term gestation) have low resting levels of CD62L (L-selectin) and do not significantly increase surface expression of CD18 after inflammatory stimulation. To determine the potential utility of preterm rabbits in investigations of perinatal human conditions, the authors compared the surface expression of the beta 2-integrin CD18 and CD62L (L-selectin) on polymorphonuclear leukocytes (PMNs) from perinatal rabbits and perinatal humans, both under resting conditions and after in vitro activation with inflammatory stimulants. Methods After erythrocyte lysis of whole-blood samples, leukocytes from 7-day-old, full-term (31-day gestation), and preterm (24-day gestation) rabbits, as well as full-term (37-42 week gestation) and preterm (27-36 week gestation) human newborns were prepared and stimulated in vitro at 37 degrees C with either C5a or phorbol myristate acetate. After fluorescence labeling of CD18 and CD62L with monoclonal antibodies, PMN adhesion molecule expression was assessed by flow cytometry. Results Constitutive CD18 expression was not significantly different between perinatal and adult humans but was reduced in all perinatal rabbits compared with adults. Inflammatory stimulation caused significant increases in CD18 expression in adult human PMNs but not in full-term and preterm newborns. Changes in CD18 expression in adult and preterm rabbits after stimulation, although in the same direction as humans, were more variable. In both species, constitutive CD62L expression on PMNs from all perinates was significantly lower than in adults. However, CD62L was shed to similar degrees after inflammatory stimulation in all groups. Conclusions Preterm rabbits may provide a potentially useful experimental model to study PMN adhesion and host defense in the perinatal period, particularly preterm gestations. Specific advantages and limitations of rabbits in such studies are discussed.

scholarly journals Interleukin-23 (IL-23)-IL-17 Cytokine Axis in Murine Pneumocystis carinii Infection

2007 ◽  
Vol 75 (6) ◽  
pp. 3055-3061 ◽  
Author(s):  
Xiaowen L. Rudner ◽  
Kyle I. Happel ◽  
Erana A. Young ◽  
Judd E. Shellito
Keyword(s):  
T Cells ◽  
Host Defense ◽  
Defense Mechanisms ◽  
Pneumocystis Carinii ◽  
Neutralizing Antibody ◽  
Wild Type ◽  
Pneumocystis Carinii Infection ◽  
Interleukin 23

ABSTRACT Host defense mechanisms against Pneumocystis carinii are not fully understood. Previous work in the murine model has shown that host defense against infection is critically dependent upon host CD4+ T cells. The recently described Th17 immune response is predominantly a function of effector CD4+ T cells stimulated by interleukin-23 (IL-23), but whether these cells are required for defense against P. carinii infection is unknown. We tested the hypothesis that P. carinii stimulates the early release of IL-23, leading to increases in IL-17 production and lung effector CD4+ T-cell population that mediate clearance of infection. In vitro, stimulation of alveolar macrophages with P. carinii induced IL-23, and IL-23p19 mRNA was expressed in lungs of mice infected with this pathogen. To address the role of IL-23 in resistance to P. carinii, IL-23p19−/− and wild-type control C57BL/6 mice were infected and their fungal burdens and cytokine/chemokine responses were compared. IL-23p19−/− mice displayed transient but impaired clearance of infection, which was most apparent 2 weeks after inoculation. In confirmatory studies, the administration of either anti-IL-23p19 or anti-IL-17 neutralizing antibody to wild-type mice infected with P. carinii also caused increases in fungal burdens. IL-17 and the lymphocyte chemokines IP-10, MIG, MIP-1α, MIP-1β, and RANTES were decreased in the lungs of infected IL-23p19−/− mice in comparison to their levels in the lungs of wild-type mice. In IL-23p19−/− mice infected with P. carinii, there were fewer effector CD4+ T cells in the lung tissue. Collectively, these studies indicate that the IL-23-IL-17 axis participates in host defense against P. carinii.

scholarly journals Staphylococcus aureus—A Known Opponent against Host Defense Mechanisms and Vaccine Development—Do We Still Have a Chance to Win?

2022 ◽  
Vol 23 (2) ◽  
pp. 948
Author(s):  
Urszula Wójcik-Bojek ◽  
Barbara Różalska ◽  
Beata Sadowska
Keyword(s):  
Staphylococcus Aureus ◽  
Antibiotic Therapy ◽  
Virulence Factors ◽  
Host Defense ◽  
Defense Mechanisms ◽  
Vaccine Development ◽  
Global Trends ◽  
Molecular Microbiology ◽  
Modern Technologies ◽  
New Vaccines

The main purpose of this review is to present justification for the urgent need to implement specific prophylaxis of invasive Staphylococcus aureus infections. We emphasize the difficulties in achieving this goal due to numerous S. aureus virulence factors important for the process of infection and the remarkable ability of these bacteria to avoid host defense mechanisms. We precede these considerations with a brief overview of the global necessitiy to intensify the use of vaccines against other pathogens as well, particularly in light of an impasse in antibiotic therapy. Finally, we point out global trends in research into modern technologies used in the field of molecular microbiology to develop new vaccines. We focus on the vaccines designed to fight the infections caused by S. aureus, which are often resistant to the majority of available therapeutic options.

scholarly journals Host defense deficiency in hairy cell leukemia and its correction by leukocyte transfusion

Blood ◽  
1980 ◽  
Vol 56 (3) ◽  
pp. 526-533 ◽  
Author(s):  
EM Hersh ◽  
S Murphy ◽  
A Zander ◽  
K Dicke ◽  
DJ Stewart ◽  
...  
Keyword(s):  
Host Defense ◽  
Hairy Cell Leukemia ◽  
Defense Mechanisms ◽  
Pokeweed Mitogen ◽  
Hairy Cell ◽  
Cell Leukemia ◽  
Con A ◽  
Dependent Cell ◽  
Monocyte Adherence

Abstract A similar defect host defense mechanisms in hairy cell leukemia was defined in two patients. Surface-adherent monocytes were not detected in the peripheral blood nor were monocytes that mediate antibody- dependent cell-mediated cytotoxicity (ADCC) to isoantibody-coated human erythrocytes. In addition, lymphocytes of both patients failed to show blastogenic responses to concanavalin A (Con-A) and pokeweed mitogen (PWM) but showed a vigorous response to phytohemagglutinin (PHA). Other immunologic abnormalities were present but were either moderate in degree or were not present in both patients. In vitro lymphocyte blastogenic responses were fully restored by incubation of patients' leukocytes with a normal donor's adherent monocytes. One patient received daily allogeneic leukocyte transfusion for 4 days. This resulted in complete normalization of monocyte adherence and ADCC that persisted for several months after transfusion and was associated with hemotalogic improvement. Therapy in case 1 resulted in correction of the blastogenic responses to Con-A and PWM. Thus, a host defense defect in hairy cell leukemia has been defined in 2 patients and a preliminary result suggests that therapy with leukocyte transfusions may be useful in the postsplenectomy patient with an infectious complication and should be explored further.

scholarly journals Tiamulin fumarat – new makrolide on bovine mastitis therapy in vivo and in vitro

2020 ◽  
Vol 17 ◽  
pp. 00203
Author(s):  
Vera Kriukova ◽  
Nadezda Kuznechova ◽  
Viktoriya Gaponova ◽  
Lilia Sabyrzyanova
Keyword(s):  
Virulence Factors ◽  
Antibacterial Effect ◽  
Bovine Mastitis ◽  
Leningrad Region ◽  
Negative Consequences ◽  
Chemotherapy Drugs ◽  
Positive Effect ◽  
Active Substances

Antibiotics nowadays are widely used for the treatment of mastitis in cows, which, along with a positive effect, cause negative consequences to the organism of an animal, can be consumed by people and interacts the cultural qualities of microorganisms However, it is almost impossible to refuse from antibacterial therapy of mastitis with chemotherapy drugs. And the variety range of chemotherapy drugs for mastitis therapy today is very wide. Since we conduct monitoring devoted to full characteristics of the strains of Streptococcus spp., isolated from bovine mastitis milk of the geographical zone of Leningrad region, Russia. That is, we analyses received data on the cultural, microbiological, serological, virulence factors, and sensibility to main used in practice antibiotics and to new ones. Taking into account the already proven resistance of microorganisms to antibiotics, the biological industry offers antibacterial drugs based on new active substances for use in the treatment of cow mastitis. In the assay described in this paper, we set a goal-to investigate the antibacterial effect of tiamulin fumarat to clinical isolates of streptococci received from milk of cows with mastitis, and to determine its clinical efficacy on cows with mastitis of the bacteriological etiology

scholarly journals Promotion of Anti-Tuberculosis Macrophage Activity by L-Arginine in the Absence of Nitric Oxide

2021 ◽  
Vol 12 ◽  
Author(s):  
Melanie C. McKell ◽  
Rebecca R. Crowther ◽  
Stephanie M. Schmidt ◽  
Michelle C. Robillard ◽  
Rachel Cantrell ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Host Defense ◽  
Defense Mechanisms ◽  
No Production ◽  
Macrophage Function ◽  
Macrophage Activity ◽  
Extracellular Stimuli ◽  
Essential Nutrient ◽  
Inhibition Of Glycolysis

Macrophages are indispensable immune cells tasked at eliminating intracellular pathogens. Mycobacterium tuberculosis (Mtb), one of the most virulent intracellular bacterial pathogens known to man, infects and resides within macrophages. While macrophages can be provoked by extracellular stimuli to inhibit and kill Mtb bacilli, these host defense mechanisms can be blocked by limiting nutritional metabolites, such as amino acids. The amino acid L-arginine has been well described to enhance immune function, especially in the context of driving macrophage nitric oxide (NO) production in mice. In this study, we aimed to establish the necessity of L-arginine on anti-Mtb macrophage function independent of NO. Utilizing an in vitro system, we identified that macrophages relied on NO for only half of their L-arginine-mediated host defenses and this L-arginine-mediated defense in the absence of NO was associated with enhanced macrophage numbers and viability. Additionally, we observed macrophage glycolysis to be driven by both L-arginine and mechanistic target of rapamycin (mTOR), and inhibition of glycolysis or mTOR reduced macrophage control of Mtb as well as macrophage number and viability in the presence of L-arginine. Our data underscore L-arginine as an essential nutrient for macrophage function, not only by fueling anti-mycobacterial NO production, but also as a central regulator of macrophage metabolism and additional host defense mechanisms.

Phagocytosis of Staphylococci Biofilms by Polymorphonuclear Neutrophils: S. aureus and S. epidermidis Differ with Regard to Their Susceptibility Towards the Host Defense

2009 ◽  
Vol 32 (9) ◽  
pp. 565-573 ◽  
Author(s):  
Frank Guenther ◽  
Petra Stroh ◽  
Christof Wagner ◽  
Ursula Obst ◽  
Gertrud Maria Hänsch
Keyword(s):  
Host Defense ◽  
Defense Mechanisms ◽  
Orthopedic Implants ◽  
Time Lapse ◽  
Polymorphonuclear Neutrophils ◽  
Bacterial Strains ◽  
Phagocytic Cells ◽  
First Line ◽  
Persistent Infections

Bacteria organized in biofilms are a common cause of relapsing or persistent infections. In patients receiving orthopedic implants, such as endoprostheses or osteosynthesis materials, Staphylococcus aureus and S. epidermidis are prevalent and it is widely assumed that bacteria in biofilms are not only relatively resistant towards antibiotics and biocides, but also towards host defense mechanisms. In that context, we addressed the question how polymorphonuclear neutrophils (PMN), the “first line defense” against bacterial infection, interact with biofilms generated in vitro. By time-lapse video microscopy, we observed migration of PMN towards the biofilms. In the case of S. aureus, the PMN moved across the biofilm and took up bacteria as they moved along. On S. epidermidis, in contrast, the PMN were rather immobile, and phagocytosis was limited to bacteria in the immediate vicinity. By labeling the bacteria within the biofilm with 3H-thymidine we found that S. aureus biofilms were more sensitive towards the PMN attack than S. epidermidis. Following phagocytosis of either bacteria strain, the PMN underwent apoptosis, in line with the dogma, that phagocytosis induces programmed cell-death in order to prevent spilling of the bactericidal and cytotoxic entities. In conclusion, biofilms are not inherently protected against the attack by phagocytic cells; their sensitivity, however, varies among bacterial strains, presumably due to properties of the extracellular biofilm matrix affecting the motility of PMN on the film.

scholarly journals Microbial Pathogenesis

2021 ◽  
Vol 11 (12) ◽  
pp. 217-219
Author(s):  
Ruvin Haidar
Keyword(s):  
Key Words ◽  
Virulence Factors ◽  
Host Defense ◽  
Defense Mechanisms ◽  
Pathogenic Microorganism ◽  
Microbial Pathogenesis ◽  
Pathological Effect ◽  
Susceptible Host ◽  
Gain Access ◽  
Pathogenic Microbe

For a pathogenic microbe to cause disease in a susceptible host, it must gain access to that host first. The pathogenicity of a microbe is determined by the virulence factors alongside other innate mechanisms. Apart from the initiation of infection, these virulence factors also enable the pathogenic microorganism to survive in the new environment within the susceptible host. They also enable the pathogenic microorganism to invade the host, colonize, and evade the host defense mechanisms. These virulence factors include; invasins, capsules, siderophores, adhesins, enzymes, endotoxins, and exotoxins. Key words: Pathogenicity factors and Pathological effect on cells.

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