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Hypersensitivity pneumonitis (HP) is an extrinsic allergic alveolitis characterized by inflammation of the interstitium, bronchioles, and alveoli of the lung that leads to granuloma formation. We previously found that activation of protein kinase D1 (PKD1) in the lungs following exposures to contributes to the acute pulmonary inflammation, IL-17A expression in the lungs, and development of HP. In the present study, we investigated whether PKD1 in myeloid-lineage cells affects the pathogenic course of the -induced HP. Mice were exposed intranasally to once or 3 times/week for 3 weeks. The protein and mRNA expression levels of cytokines/chemokines were detected by enzyme-linked immunosorbent assay and quantitative real-time PCR, respectively. Flow cytometry was used to detect the different types of immune cells and the levels of surface proteins. Lung tissue sections were stained with hematoxylin and eosin, digital images were captured, and immune cells influx into the interstitial lung tissue were detected. Compared to control PKD1-sufficient mice, mice with PKD1 deficiency in myeloid-lineage cells (PKD1mKO) showed significantly suppressed expression of TNFα, IFNγ, IL-6, CCL2, CCL3, CCL4, CXCL1, CXCL2, and CXCL10 and neutrophilic alveolitis after single intranasal exposure to . Substantially reduced levels of alveolitis and granuloma formation were observed in the PKD1mKO mice repeatedly exposed to for 3 weeks. In addition, expression levels of the Th1/Th17 polarizing cytokines and chemokines such as IFNγ, IL-17A, CXCL9, CXCL10, CXCL11, and CCL20 in lungs were significantly reduced in the PKD1mKO mice repeatedly exposed to . Moreover, accumulation of CXCR3+CCR6+ nonconventional Th1 in the lungs were significantly reduced in PKD1mKO mice repeatedly exposed to . Our results demonstrate that PKD1 in myeloid-lineage cells plays an essential role in the development and progress of HP caused by repeated exposure to by contributing Th1/Th17 polarizing proinflammatory responses, alveolitis, and accumulation of pathogenic nonconventional Th1 cells in the lungs.

[This corrects the article DOI: 10.3389/fimmu.2024.1403155.].

Ecosystem services (ES) are becoming a burgeoning topic presently playing a crucial role in sustaining human well-being, socioeconomic growth, and addressing environmental management and sustainability. The purpose of our review was to overview research trends of the forest ecosystem services (FES) in eastern India and the research methodologies adopted to evaluate them. To systematically study the FES literature, 127 articles pertaining to the term FES during the period 1991 to 2021 were reviewed through a quantitative analysis. The analytical outcome emphasized (1) the research aspects of FES and its types along with regional distribution, (2) the scenario of FES in eastern India with respect to other ES and India, (3) the quantitative trend of FES research over 30 years period, (4) the employed methodological approaches, and (5) the existing research gaps and prospects. Our findings suggest that the publication numbers are quite low in eastern India, as only 5 peer-reviewed articles were found on FES. The result also indicated that the majority of studies primarily focused on provisioning services (85.03%) and the survey/interview method gained more popularity as a primary data source. Most of the earlier studies employed basic assessments like product values or individual income. We also discussed the advantages as well as limitations of the employed methodologies. These findings further highlight the significance of valuing various FES collectively rather than individually and contribute to providing pertinent information for the FES literature scenario, which may help to strengthen forest management as well.

Background: The Indian elephant (Elephas maximus indicus), a subspecies of the Asian elephant, is predominantly found in India, supporting nearly 60% of the global population. In West Bengal state, particularly in the northern districts (Darjeeling, Jalpaiguri, and Alipurduar) unremitting habitat destruction, encroachment, and high population densities of both humans and elephants have led to an escalation in human-elephant conflicts (HECs). Among different mitigation measures, electric fences (EFs) are commonly preferred, however, illegal usage of lethal EFs has led to increased cases of electrocution-based elephant mortalities. Aims: A study was conducted at selected HEC-prone sites in elephant habitats of the northern districts to (i) document the physical status of EFs installed, (ii) examine local community perceptions regarding the efficacy of EFs in mitigating elephant raids, and (iii) provide recommendations for the sustainable management of EFs. Methods: Firstly, secondary data (2017–2023) on elephant electrocution incidents were collected from literature, official records, and media sources from the study area. Based on this, EFs were assessed at 33 conflict-prone sites across various land-use types. Subsequently, semi-structured interviews were conducted with 166 randomly selected residents within 5 km of the fence sites to assess their perceptions regarding efficacy of EFs. Statistical analyses were executed to analyse associations between fence characteristics, land-use, and socio-demographic factors. Results: Of the 62 fences assessed, 32 were active and 14 were found to be lethal. The findings revealed non-lethal fences were more prevalent than lethal ones, indicating a growing awareness within local communities about the adverse impacts of lethal EFs. The perception-based survey revealed that 39.8% of respondents considered EFs moderately effective in mitigating conflicts. Implication for Conservation: While mass-awareness has shown promising results, policymakers are recommended to implement stricter regulations and establish region-specific monitoring squads.

Human-elephant conflicts (HECs) have surged worldwide due to widespread forest habitat destruction and human encroachment. In India, where only a small portion of elephant habitats are protected, these conflicts are particularly severe. West Bengal, with its substantial elephant population, faces significant challenges in addressing HECs, especially in its southern regions where conflict incidences are increasing in recent times. This study aims to elucidate the perceptions of local inhabitants residing in and around conflict-prone zones of elephant habitats in southern West Bengal. A structured questionnaire was employed to gather insights from 204 individuals across four administrative districts in the western part of south West Bengal. Results revealed that socio-economic and demographic factors greatly influence attitudes towards conservation. Despite diverse mitigation practices in response to challenges like crop damage and property loss, dissatisfaction with compensation schemes persists. These findings underscore the complexity of human-elephant interactions in the region and emphasize the need for holistic approaches that consider both conservation and livelihood needs.

mTOR plays a crucial role in cell growth by controlling ribosome biogenesis, metabolism, autophagy, mRNA translation, and cytoskeleton organization. It is a serine/threonine kinase that is part of two distinct extensively described protein complexes, mTORC1 and mTORC2. We have identified a rapamycin-resistant mTOR complex, called mTORC3, which is different from the canonical mTORC1 and mTORC2 complexes in that it does not contain the Raptor, Rictor, or mLST8 mTORC1/2 components. mTORC3 phosphorylates mTORC1 and mTORC2 targets and contains the ETS transcription factor ETV7, which binds to mTOR and is essential for mTORC3 assembly in the cytoplasm. Tumor cells that assemble mTORC3 have a proliferative advantage and become resistant to rapamycin, indicating that inhibiting mTORC3 may have a therapeutic impact on cancer. Here, we investigate which domains or amino acid residues of ETV7 and mTOR are involved in their mutual binding. We found that the mTOR FRB and LBE sequences in the kinase domain interact with the pointed (PNT) and ETS domains of ETV7, respectively. We also found that forced expression of the mTOR FRB domain in the mTORC3-expressing, rapamycin-resistant cell line Karpas-299 out-competes mTOR for ETV7 binding and renders these cells rapamycin-sensitive in vivo. Our data provide useful information for the development of molecules that prevent the assembly of mTORC3, which may have therapeutic value in the treatment of mTORC3-positive cancer.

Summary Autophagy is an intracellular catabolic process that is required to maintain cellular homeostasis. Pathogen‐elicited host cell autophagy may favour containment of infection or may help in bacterial survival. Pathogens have developed the ability to modulate host autophagy. The secreted antigen HP0175, a peptidyl prolyl cis,trans isomerase of Helicobacter pylori, has moonlighting functions with reference to host cells. Here we show that it executes autophagy in gastric epithelial cells. Autophagy is dependent on the unfolded protein response (UPR) that activates the expression of PKR‐like ER kinase (PERK). This is accompanied by phosphorylation of eukaryotic initiation factor 2α (eIF‐2α) and transcriptional activation of ATF4 and CHOP. Knockdown of UPR‐related genes inhibits the conversion of LC3I to LC3II, a marker of autophagy. The autophagy‐inducing ability of H. pylori is compromised when cells are infected with an isogenic hp0175 mutant. Autophagy precedes apoptosis. Silencing of BECLIN1 augments cleavage of caspase 3 as well as apoptosis. Increased apoptosis of gastric epithelial cells is known to be linked to H. pylori‐mediated gastric inflammation and carcinogenesis. To the best of our knowledge, this study provides the first demonstration of how HP0175 endowed with moonlighting functions links UPR‐dependent autophagy and apoptosis during H. pylori infection.

Despite the recent advances in diagnostic and therapeutic strategies, oral squamous cell carcinoma (OSCC) remains a major health burden. Protein biomarker discovery for early detection will help to improve patient survival rate in OSCC. Mass spectrometry-based proteomics has emerged as an excellent approach for detection of protein biomarkers in various types of cancers. In the current study, we have used 4-Plex isobaric tags for relative and absolute quantitation (iTRAQ)-based shotgun quantitative proteomic approach to identify proteins that are differentially expressed in cancerous tissues compared to normal tissues. The high-resolution mass spectrometric analysis resulted in identifying 2,074 proteins, among which 288 proteins were differentially expressed. Further, it was noticed that 162 proteins were upregulated, while 125 proteins were downregulated in OSCC-derived cancer tissue samples as compared to the adjacent normal tissues. We identified some of the known molecules which were reported earlier in OSCC such as MMP-9 (8.4-fold), ZNF142 (5.6-fold), and S100A7 (3.5-fold). Apart from this, we have also identified some novel signature proteins which have not been reported earlier in OSCC including ras-related protein Rab-2A isoform, RAB2A (4.6-fold), and peroxiredoxin-1, PRDX1 (2.2-fold). The immunohistochemistry-based validation using tissue microarray slides in OSCC revealed overexpression of the RAB2A and PRDX1 gene in 80 and 68 % of the tested clinical cases, respectively. This study will not only serve as a resource of candidate biomarkers but will contribute towards the existing knowledge on the role of the candidate molecules towards disease progression and therapeutic potential.

mTOR plays a crucial role in cell growth by controlling ribosome biogenesis, metabolism, autophagy, mRNA translation, and cytoskeleton organization. It is a serine/threonine kinase that is part of two distinct extensively described protein complexes, mTORC1 and mTORC2. We have identified a rapamycin resistant mTOR complex, called mTORC3, which is different from the canonical mTORC1 and mTORC2 complexes in that it does not contain the Raptor, Rictor, or mLST8 mTORC1 / 2 components. mTORC3 phosphorylates mTORC1 and mTORC2 targets and contains the ETS transcription factor ETV7, which binds to mTOR and is essential for mTORC3 assembly in the cytoplasm. Tumor cells that assemble mTORC3 have a proliferative advantage and become resistant to rapamycin, indicating that inhibiting mTORC3 may have a therapeutic impact on cancer. Here, we investigate which domains or amino acid residues of ETV7 and mTOR are involved in their mutual binding. We found that the mTOR FRB and LBE sequences in the kinase domain interact with the pointed (PNT) and ETS domains of ETV7, respectively. We also found that forced expression of the mTOR FRB domain in the mTORC3 expressing, rapamycin-resistant cell line Karpas-299 out competes mTOR for ETV7 binding and renders these cells rapamycin-sensitive in vivo. Our data provide useful information for the development of molecules that prevent the assembly of mTORC3, which may have therapeutic value in the treatment of mTORC3 positive cancer.