Biology subjects

Jamali, H.

Publications and source records attributed to Jamali, H..

3 recordsLinked to original sources

bioRxiv2026

Regulation of PL fimbriae (plf) and role of PlfB as a negative regulator during avian pathogenic Escherichia coli infection in turkeys

Little is currently known about the regulation of PL fimbriae produced by some pathogenic E. coli strains. We identified PlfB, a transcriptional regulator of the PapB family, as a negative regulator of PL fimbriae (Plf). Deletion of plfB significantly increased plfA transcription and Plf production. PlfB bound specifically to the plfA promoter region. Using a PplfA-lux reporter system, the deletion of plfB caused sustained and increased expression across serial passages. Global regulatory genes such as lrp, argR, and hns were also implicated in regulation of plf expression. Loss of lrp or argR decreased plf expression, suggesting these regulators positively regulate PL fimbriae. By contrast, loss of hns increased levels of plf expression, supporting its role as a negative regulator. Interestingly, loss of plfB significantly increased bacterial colonization in the lung of 6-day-old turkey poults. Further, complementation of plfB restored plf fimbrial expression and colonization of turkey lungs to wild-type levels. This further supports an important role for PL fimbriae for colonization of turkey lungs, since loss of plfB which resulted in increased plf gene expression in turkey lungs also correlated with higher bacterial numbers in the lungs. Taken together, these results indicate that PlfB acts as a negative regulator to reduce levels of PL fimbrial expression, under some conditions, but that it is not required for plf expression. This contrasts with the role the PapB regulator, which has been shown to play an essential role in expression of P fimbriae in uropathogenic E. coli strains.

microbiology↗

bioRxiv2025

Host range and zoonotic potential linked to P-like fimbrial adhesin specificity in avian pathogenic Escherichia coli

Fimbrial adhesins are surface-associated bacterial proteins that contribute to colonization, tissue tropism, and biofilm formation. Genomic analysis of the avian pathogenic Escherichia coli (APEC) strain QT598 identified a plasmid-localized fimbrial operon, termed plf which encodes P-like (PL) fimbriae. Herein, we investigated the role of P-like (PL) fimbriae, encoded on the ColV plasmid of APEC strain QT598, in a natural host turkey respiratory infection model. We determined that deletion of the plf genes reduced colonization in the lungs of turkeys. The PlfG class II fimbrial adhesin from APEC strain QT598 demonstrated species- and tissue-specific adherence, as adherence to turkey lung sections in vitro was more pronounced than adherence to chicken lung sections. In vivo, expression of plf was also found to be upregulated in the lungs of turkeys during infection, as determined by qRT-PCR. Glycan array analysis showed that the PlfG class II adhesin recognizes Lewis b, Lewis y, and H antigens as potential receptors that are present on human red blood cells and on the surface of turkey respiratory tissues, implicating specific -1,2-linked glycans as receptors. Structural modelling of Plf adhesin revealed conserved {beta}-sandwich folds with distinct binding pockets that predict receptor specificity differences between Plf adhesin variants and other fimbrial adhesins such as PapG II and the PlfG class I adhesin from UMEA 3703-1. These findings highlight the role of PL fimbriae in APEC virulence and suggest a potential zoonotic and foodborne risk from poultry to humans, demonstrating the common recognition of glycans present on both turkey and mammalian host cells and tissues. Author summaryFimbrial adhesins may play a role in bacterial attachment and colonization of host cells. We examined the role of new pap-like (PL) fimbriae in an Avian Pathogenic E. coli (APEC) strain originally isolated from a systemic infection in a young turkey poult using genetic, molecular, and cell culture methods, as well as a turkey infection model. Deletion of plf genes also decreased colonization in the turkeys lungs, and comparison between the wild-type APEC isolate and the plf-mutant showed that these fimbriae strongly promote adherence to turkey lung sections compared to chicken lung sections. The PL fimbrial adhesin of strain QT598 demonstrated receptor-specificity to fucose [a]-1,2-galactose containing glycans, including Lewis b, Lewis y, and H antigens or similar glycans as determined by carbohydrate inhibition and glycan array experiments. These findings highlight the role of PL fimbriae in APEC virulence and suggest a potential zoonotic and foodborne risk from poultry to humans, demonstrating the common recognition of glycans present on both turkey and mammalian host cells and tissues.

microbiology↗

bioRxiv2021

Free for all, or free-for-all? A content analysis of Australian university open access policies

Recent research demonstrates that Australia lags in providing open access to research outputs. In Australia, while the two major research funding bodies require open access of outputs from projects they fund, these bodies only fund a small proportion of research conducted. The major source of research and experimental development funding in Australian higher education is general university, or institutional, funding, and such funds are not subject to national funder open access policies. Thus, institutional policies and other institutional supports for open access are important in understanding Australias OA position. The purpose of this paper is, therefore, to understand the characteristics of Australian institutional open access policies and to explore the extent they represent a coherent and unified approach to delivering and promoting open access in Australia. Open access policies were located using a systematic web search approach and then their contents were analysed. Only half of Australian universities were found to have an open access policy. There was a wide variation in language used, expressed intent of the policy and expectations of researchers. Few policies mention monitoring or compliance and only three mention consequences for non-compliance. While it is understandable that institutions develop their own policies, when language is used which does not reflect national and international understandings, when requirements are not clear and with consequences, policies are unlikely to contribute to understanding of open access, to uptake of the policy, or to ease of transferring understanding and practices between institutions. A more unified approach to open access is recommended.

scientific communication and education↗