scholarly journals Variability of defensin genes from a Mexican endemic Triatominae: Triatoma (Meccus) pallidipennis (Hemiptera: Reduviidae)

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Paulina Díaz-Garrido ◽  
Omar Sepúlveda-Robles ◽  
Ignacio Martínez-Martínez ◽  
Bertha Espinoza
Keyword(s):  
Health Problem ◽  
Immune Defense ◽  
Cationic Peptides ◽  
Insect Vector ◽  
Mature Peptide ◽  
Genes Encoding ◽  
Insect Defensin ◽  
Mode Of Transmission ◽  
Meccus Pallidipennis

Chagas disease remains a serious health problem for countries where the most common mode of transmission is infection contracted from the feces of a Triatominae insect vector. In México, 32 species of Triatoma have been identified; amongst them, Triatoma (Meccus) pallidipennis is an endemic species reported to have high percentages of infection with T. cruzi. Defensins, cysteine-rich cationic peptides, are a family of antimicrobial peptides (AMPs); the synthesis of these molecules is crucial for insect’s immune defense. In the present study, the genes encoding defensins in T. pallidipennis were sequenced with the purpose of identifying the variability of these genes in a Mexican vector of T. cruzi. We found 12 different genes encoding three mature peptides, all of which had the typical folding of a functional insect defensin. In this work two Defensins type 1 and one type 4 were identified. The pro-peptide domain was highly variable and the mature peptide was not. This is the first report focus on variability of defensins from an epidemiologically important Triatoma in Mexico.

Isolation and characterization of the genes encoding antimicrobial neutrophil cationic peptides, defensins.

Ensho ◽  
1995 ◽  
Vol 15 (1) ◽  
pp. 33-41
Author(s):  
Isao Nagaoka ◽  
Noriko Ishihara ◽  
Akimasa Someya ◽  
Kazuhisa Iwabuchi ◽  
Shin Yomogida ◽  
...  
Keyword(s):  
Cationic Peptides ◽  
Isolation And Characterization ◽  
Genes Encoding

scholarly journals Intra- and Interspecies Signaling betweenStreptococcus salivarius and Streptococcus pyogenes Mediated by SalA and SalA1 Lantibiotic Peptides

2001 ◽  
Vol 183 (13) ◽  
pp. 3931-3938 ◽  
Author(s):  
M. Upton ◽  
J. R. Tagg ◽  
P. Wescombe ◽  
H. F. Jenkinson
Keyword(s):  
Streptococcus Pyogenes ◽  
Response Regulator ◽  
Genetic Locus ◽  
Two Component System ◽  
Peptide Modification ◽  
Insertional Inactivation ◽  
Two Component ◽  
Genes Encoding ◽  
Dose Dependent

ABSTRACT Streptococcus salivarius 20P3 produces a 22-amino-acid residue lantibiotic, designated salivaricin A (SalA), that inhibits the growth of a range of streptococci, including all strains ofStreptococcus pyogenes. Lantibiotic production is associated with the sal genetic locus comprisingsalA, the lantibiotic structural gene; salBCTXgenes encoding peptide modification and export machinery proteins; andsalYKR genes encoding a putative immunity protein and two-component sensor-regulator system. Insertional inactivation ofsalB in S. salivarius 20P3 resulted in abrogation of SalA peptide production, of immunity to SalA, and ofsalA transcription. Addition of exogenous SalA peptide tosalB mutant cultures induced dose-dependent expression ofsalA mRNA (0.2 kb), demonstrating that SalA production was normally autoregulated. Inactivation of salR encoding the response regulator of the SalKR two-component system led to reduced production of, and immunity to, SalA. The sal genetic locus was also present in S. pyogenes SF370 (M type 1), but because of a deletion across the salBCT genes, the corresponding lantibiotic peptide, designated SalA1, was not produced. However, in S. pyogenes T11 (M type 4) the sallocus gene complement was apparently complete, and active SalA1 peptide was synthesized. Exogenously added SalA1 peptide from S. pyogenes T11 induced salA1 transcription in S. pyogenes SF370 and in an isogenic S. pyogenes T11salB mutant and salA transcription in S. salivarius 20P3 salB. Thus, SalA and SalA1 are examples of streptococcal lantibiotics whose production is autoregulated. These peptides act as intra- and interspecies signaling molecules, modulating lantibiotic production and possibly influencing streptococcal population ecology in the oral cavity.

scholarly journals Virulent Shigella flexneri subverts the host innate immune response through manipulation of antimicrobial peptide gene expression

2008 ◽  
Vol 205 (5) ◽  
pp. 1121-1132 ◽  
Author(s):  
Brice Sperandio ◽  
Béatrice Regnault ◽  
Jianhua Guo ◽  
Zhi Zhang ◽  
Samuel L. Stanley ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Shigella Flexneri ◽  
Host Cells ◽  
Virulence Plasmid ◽  
Cationic Peptides ◽  
Immunity Genes ◽  
Genes Encoding ◽  
Peptide Gene

Antimicrobial factors are efficient defense components of the innate immunity, playing a crucial role in the intestinal homeostasis and protection against pathogens. In this study, we report that upon infection of polarized human intestinal cells in vitro, virulent Shigella flexneri suppress transcription of several genes encoding antimicrobial cationic peptides, particularly the human β-defensin hBD-3, which we show to be especially active against S. flexneri. This is an example of targeted survival strategy. We also identify the MxiE bacterial regulator, which controls a regulon encompassing a set of virulence plasmid-encoded effectors injected into host cells and regulating innate signaling, as being responsible for this dedicated regulatory process. In vivo, in a model of human intestinal xenotransplant, we confirm at the transcriptional and translational level, the presence of a dedicated MxiE-dependent system allowing S. flexneri to suppress expression of antimicrobial cationic peptides and promoting its deeper progression toward intestinal crypts. We demonstrate that this system is also able to down-regulate additional innate immunity genes, such as the chemokine CCL20 gene, leading to compromised recruitment of dendritic cells to the lamina propria of infected tissues. Thus, S. flexneri has developed a dedicated strategy to weaken the innate immunity to manage its survival and colonization ability in the intestine.

scholarly journals Transcriptional regulatory networks that promote and restrict identities and functions of intestinal innate lymphoid cells

2018 ◽  
Author(s):  
Maria Pokrovskii ◽  
Jason A. Hall ◽  
David E. Ochayon ◽  
Ren Yi ◽  
Natalia S. Chaimowitz ◽  
...  
Keyword(s):  
Regulatory Networks ◽  
Inflammatory Diseases ◽  
Innate Lymphoid Cells ◽  
Chromatin Accessibility ◽  
Immune Defense ◽  
Lymphoid Cells ◽  
Transcriptional Regulatory Networks ◽  
Transcriptional Regulatory

SummaryInnate lymphoid cells (ILCs) can be subdivided into several distinct cytokine-secreting lineages that promote tissue homeostasis and immune defense but also contribute to inflammatory diseases. Accumulating evidence suggests that ILCs, similarly to other immune populations, are capable of phenotypic and functional plasticity in response to infectious or environmental stimuli. Yet the transcriptional circuits that control ILC identity and function are largely unknown. Here we integrate gene expression and chromatin accessibility data to infer transcriptional regulatory networks within intestinal type 1, 2, and 3 ILCs. We predict the “core” sets of transcription-factor (TF) regulators driving each ILC subset identity, among which only a few TFs were previously known. To assist in the interpretation of these networks, TFs were organized into cooperative clusters, or modules that control gene programs with distinct functions. The ILC network reveals extensive alternative-lineage-gene repression, whose regulation may explain reported plasticity between ILC subsets. We validate new roles for c-MAF and BCL6 as regulators affecting the type 1 and type 3 ILC lineages. Manipulation of TF pathways identified here might provide a novel means to selectively regulate ILC effector functions to alleviate inflammatory disease or enhance host tolerance to pathogenic microbes or noxious stimuli. Our results will enable further exploration of ILC biology, while our network approach will be broadly applicable to identifying key cell state regulators in otherin vivocell populations.

scholarly journals Hyperinvasiveness ofListeria monocytogenessequence type 1 is independent of lineage I‐specific genes encoding internalin‐like proteins

2019 ◽  
Vol 8 (7) ◽  
Author(s):  
Bulent Gözel ◽  
Camille Monney ◽  
Lisandra Aguilar‐Bultet ◽  
Sebastian Rupp ◽  
Joachim Frey ◽  
...  
Keyword(s):  
Genes Encoding

Polymorphisms in the Genes Encoding TGF-β1, TNF-α, and IL-6 Show Association with Type 1 Diabetes Mellitus in the Slovak Population

2010 ◽  
Vol 58 (5) ◽  
pp. 385-393 ◽  
Author(s):  
Juraj Javor ◽  
Stanislav Ferencik ◽  
Maria Bucova ◽  
Martina Stuchlikova ◽  
Emil Martinka ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Slovak Population ◽  
Tnf Α ◽  
Genes Encoding ◽  
Tgf Β1

scholarly journals Decreased Expression of Type 1 Fimbriae by apstMutant of Uropathogenic Escherichia coli Reduces Urinary Tract Infection

2012 ◽  
Vol 80 (8) ◽  
pp. 2802-2815 ◽  
Author(s):  
Sébastien Crépin ◽  
Sébastien Houle ◽  
Marie-Ève Charbonneau ◽  
Michaël Mourez ◽  
Josée Harel ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Bacterial Virulence ◽  
Pho Regulon ◽  
Upec Strain ◽  
Content Type ◽  
Type 1 Fimbriae ◽  
Genes Encoding ◽  
Tract Infections

ABSTRACTThepstSCAB-phoUoperon encodes the phosphate-specific transport system (Pst). Loss of Pst constitutively activates the Pho regulon and decreases bacterial virulence. However, specific mechanisms underlying decreased bacterial virulence through inactivation of Pst are poorly understood. In uropathogenicEscherichia coli(UPEC) strain CFT073, inactivation ofpstdecreased urinary tract colonization in CBA/J mice. Thepstmutant was deficient in production of type 1 fimbriae and showed decreased expression of thefimAstructural gene which correlated with differential expression of thefimB,fimE,ipuA, andipbAgenes, encoding recombinases, mediating inversion of thefimpromoter. The role offimdownregulation in attenuation of thepstmutant was confirmed using afimphase-locked-on derivative, which demonstrated a significant gain in virulence. In addition, thepstmutant was less able to invade human bladder epithelial cells. Since type 1 fimbriae contribute to UPEC virulence by promoting colonization and invasion of bladder cells, the reduced bladder colonization by thepstmutant is predominantly attributed to downregulation of these fimbriae. Elucidation of mechanisms mediating the control of type 1 fimbriae through activation of the Pho regulon in UPEC may open new avenues for therapeutics or prophylactics against urinary tract infections.

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