scholarly journals Infectious Keratitis: Secreted Bacterial Proteins That Mediate Corneal Damage

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Mary E. Marquart ◽  
Richard J. O'Callaghan
Keyword(s):  
Host Cell ◽  
Bacterial Infections ◽  
Cell Surface Molecules ◽  
Bacterial Proteins ◽  
Surface Molecules ◽  
Host Cell Death ◽  
Common Causes ◽  
Host Cell Surface ◽  
Stromal Collagen ◽  
Corneal Damage

Ocular bacterial infections are universally treated with antibiotics, which can eliminate the organism but cannot reverse the damage caused by bacterial products already present. The three very common causes of bacterial keratitis—Pseudomonas aeruginosa,Staphylococcus aureus, andStreptococcus pneumoniae—all produce proteins that directly or indirectly cause damage to the cornea that can result in reduced vision despite antibiotic treatment. Most, but not all, of these proteins are secreted toxins and enzymes that mediate host cell death, degradation of stromal collagen, cleavage of host cell surface molecules, or induction of a damaging inflammatory response. Studies of these bacterial pathogens have determined the proteins of interest that could be targets for future therapeutic options for decreasing corneal damage.

Burkholderia pseudomallei-induced cell fusion in U937 macrophages can be inhibited by monoclonal antibodies against host cell surface molecules

2011 ◽  
Vol 13 (12-13) ◽  
pp. 1006-1011 ◽  
Author(s):  
Supaporn Suparak ◽  
Veerachat Muangsombut ◽  
Donporn Riyapa ◽  
Joanne M. Stevens ◽  
Mark P. Stevens ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Cell Surface ◽  
Host Cell ◽  
Cell Fusion ◽  
Burkholderia Pseudomallei ◽  
Cell Surface Molecules ◽  
Surface Molecules ◽  
Host Cell Surface

Characterization of the parasite-host cell interactions involved inTheileria parvasporozoite invasion of bovine lymphocytes

Parasitology ◽  
1996 ◽  
Vol 113 (3) ◽  
pp. 267-277 ◽  
Author(s):  
M. K. Shaw
Keyword(s):  
Host Cell ◽  
De Novo ◽  
Experimental Conditions ◽  
Surface Molecules ◽  
Lymphocyte Surface ◽  
Host Cell Interactions ◽  
Host Cell Surface ◽  
Ph Dependent ◽  
Bovine Lymphocytes

SUMMARYSporozoite invasion of bovine lymphocytes byTheileria parvais a pH-dependent process that occurs without the need forde novoprotein synthesis. The process was inhibited by RGD(S) peptides, fibronectin and, in the presence of serum, by antibodies reactive with fibronectin. Invasion was also blocked by a range of sulphated glycoconjugates, but treatment of lymphocytes with heparitinase did not inhibit entry. Enzymic modifications of the lymphocyte surface demonstrated that trypsin-insensitive glycoproteins containingO- andN-linked carbohydrates as well as phospholipase-sensitive molecules on the host cell surface were critical to sporozoite entry. Modification of the lymphocyte surface with NEM and DTT had only marginal effects on sporozoite binding but blocked parasite internalization. Invasion was also blocked by several antibodies which cross-reacted with sporozoite surface molecules. While only a few experimental conditions specifically blocked sporozoite binding, a wider range of reagents and treatments inhibited parasite entry. The reasons for this are discussed in terms of the nature of the zippering process that facilitates sporozoite internalization.

scholarly journals A Single-Pass Type I Membrane Protein from the Apicomplexan Parasite Cryptosporidium parvum with Nanomolar Binding Affinity to Host Cell Surface

2021 ◽  
Vol 9 (5) ◽  
pp. 1015
Author(s):  
Tianyu Zhang ◽  
Xin Gao ◽  
Dongqiang Wang ◽  
Jixue Zhao ◽  
Nan Zhang ◽  
...  
Keyword(s):  
Membrane Protein ◽  
Cell Surface ◽  
Host Cell ◽  
Binding Affinity ◽  
Cryptosporidium Parvum ◽  
Host Cells ◽  
Watery Diarrhea ◽  
Type I ◽  
Single Pass ◽  
Host Cell Surface

Cryptosporidium parvum is a globally recognized zoonotic parasite of medical and veterinary importance. This parasite mainly infects intestinal epithelial cells and causes mild to severe watery diarrhea that could be deadly in patients with weakened or defect immunity. However, its molecular interactions with hosts and pathogenesis, an important part in adaptation of parasitic lifestyle, remain poorly understood. Here we report the identification and characterization of a C. parvum T-cell immunomodulatory protein homolog (CpTIPH). CpTIPH is a 901-aa single-pass type I membrane protein encoded by cgd5_830 gene that also contains a short Vibrio, Colwellia, Bradyrhizobium and Shewanella (VCBS) repeat and relatively long integrin alpha (ITGA) N-terminus domain. Immunofluorescence assay confirmed the location of CpTIPH on the cell surface of C. parvum sporozoites. In congruence with the presence of VCBS repeat and ITGA domain, CpTIPH displayed high, nanomolar binding affinity to host cell surface (i.e., Kd(App) at 16.2 to 44.7 nM on fixed HCT-8 and CHO-K1 cells, respectively). The involvement of CpTIPH in the parasite invasion is partly supported by experiments showing that an anti-CpTIPH antibody could partially block the invasion of C. parvum sporozoites into host cells. These observations provide a strong basis for further investigation of the roles of CpTIPH in parasite-host cell interactions.

scholarly journals Pathogen induced subversion of NAD+ metabolism mediating host cell death: a target for development of chemotherapeutics

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Ayushi Chaurasiya ◽  
Swati Garg ◽  
Ashish Khanna ◽  
Chintam Narayana ◽  
Ved Prakash Dwivedi ◽  
...  
Keyword(s):  
Cell Death ◽  
Host Cell ◽  
Nicotinamide Adenine Dinucleotide ◽  
Malaria Parasite ◽  
Host Cells ◽  
Nicotinamide Adenine ◽  
Targeted Therapeutics ◽  
Nad Metabolism ◽  
Host Cell Death ◽  
Nanomolar Range

AbstractHijacking of host metabolic status by a pathogen for its regulated dissemination from the host is prerequisite for the propagation of infection. M. tuberculosis secretes an NAD+-glycohydrolase, TNT, to induce host necroptosis by hydrolyzing Nicotinamide adenine dinucleotide (NAD+). Herein, we expressed TNT in macrophages and erythrocytes; the host cells for M. tuberculosis and the malaria parasite respectively, and found that it reduced the NAD+ levels and thereby induced necroptosis and eryptosis resulting in premature dissemination of pathogen. Targeting TNT in M. tuberculosis or induced eryptosis in malaria parasite interferes with pathogen dissemination and reduction in the propagation of infection. Building upon our discovery that inhibition of pathogen-mediated host NAD+ modulation is a way forward for regulation of infection, we synthesized and screened some novel compounds that showed inhibition of NAD+-glycohydrolase activity and pathogen infection in the nanomolar range. Overall this study highlights the fundamental importance of pathogen-mediated modulation of host NAD+ homeostasis for its infection propagation and novel inhibitors as leads for host-targeted therapeutics.

scholarly journals Mbov_0503 Encodes a Novel Cytoadhesin that Facilitates Mycoplasma bovis Interaction with Tight Junctions

2020 ◽  
Vol 8 (2) ◽  
pp. 164 ◽  
Author(s):  
Xifang Zhu ◽  
Yaqi Dong ◽  
Eric Baranowski ◽  
Xixi Li ◽  
Gang Zhao ◽  
...  
Keyword(s):  
Host Cell ◽  
Tight Junctions ◽  
Binding Capacity ◽  
Host Cells ◽  
Mycoplasma Bovis ◽  
Knock Out ◽  
Cell Monolayers ◽  
Protein Levels ◽  
Complex Process ◽  
Host Cell Surface

Molecules contributing to microbial cytoadhesion are important virulence factors. In Mycoplasma bovis, a minimal bacterium but an important cattle pathogen, binding to host cells is emerging as a complex process involving a broad range of surface-exposed structures. Here, a new cytoadhesin of M. bovis was identified by producing a collection of individual knock-out mutants and evaluating their binding to embryonic bovine lung cells. The cytoadhesive-properties of this surface-exposed protein, which is encoded by Mbov_0503 in strain HB0801, were demonstrated at both the mycoplasma cell and protein levels using confocal microscopy and ELISA. Although Mbov_0503 disruption was only associated in M. bovis with a partial reduction of its binding capacity, this moderate effect was sufficient to affect M. bovis interaction with the host-cell tight junctions, and to reduce the translocation of this mycoplasma across epithelial cell monolayers. Besides demonstrating the capacity of M. bovis to disrupt tight junctions, these results identified novel properties associated with cytoadhesin that might contribute to virulence and host colonization. These findings provide new insights into the complex interplay taking place between wall-less mycoplasmas and the host-cell surface.

scholarly journals Cell surface molecules that bind fibronectin's matrix assembly domain

1991 ◽  
Vol 266 (15) ◽  
pp. 9697-9702 ◽  
Author(s):  
A.H. Limper ◽  
B.J. Quade ◽  
R.M. LaChance ◽  
T.M. Birkenmeier ◽  
T.S. Rangwala ◽  
...  
Keyword(s):  
Cell Surface ◽  
Cell Surface Molecules ◽  
Matrix Assembly ◽  
Surface Molecules
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