bioRxiv Science⌕ Search

bioRxiv · 10.1101/2021.07.28.454186

Submandibular Injection of Indoleamine 2,3-Dioxygenase Galectin-3 Fusion Protein Inhibits and Prevents Periodontal Disease Progression Over 12 Weeks

Abstract

AO_SCPLOWBSTRACTC_SCPLOWA major challenge in the treatment of chronic inflammatory diseases including periodontal diseases is the development of therapeutics to safely and specifically direct resolution of inflammation in a localized manner. Here we demonstrate the efficacy of a novel approach that addresses this unmet clinical need. Using an enzyme fusion protein of indoleamine 2,3-dioxygenase 1 (IDO) and galectin-3 (Gal3) with tissue-anchored and thus localized immunomodulatory properties, we prevented and halted progression of induced polymicrobial periodontal disease. Efficacy was achieved with repeated treatment with IDO-Gal3 and was measured by effects on mandibular bone loss, soft tissue inflammation and local T cell plasticity. Specifically, both prophylactic and therapeutic administration of IDO-Gal3 were effective in reducing vertical mandibular bone loss and loss of mandibular bone volume and bone thickness induced by chronic polymicrobial infection. The efficacy observed is at least in part due to localized regulation of innate immune mediators such as IL-1{beta}, IL-6 and IL-8 as well as chemoattractants including IP-10, MCP-1 and MIP-1, while enhancing the expression of immunoregulatory cytokines such as IL-10. In addition, IDO-Gal3 treatment suppressed the induction of pathogenic CD4+Th1, CD8+Tc1, CD4+Th1/Th17, and CD8+Tc1/Tc17, while promoting the induction of homeostatic CD4+Th17, CD8+Tc17 and CD4+Tregs. Importantly, the efficacy of prophylactically and therapeutically administered IDO-Gal-3 is not dependent on bacterial burden as there were no appreciable effects on bacterial burden following either method of administration. Lastly, therapeutic rather than prophylactic administration of IDO-Gal3 is most effective in preventing mandibular bone loss through more robust innate and adaptive immune modulation. Together these and our previously published data indicate that therapeutic administration of IDO-Gal3 addresses the clinical needs for adjunctive therapeutics to treat active and/or established periodontal diseases.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Rocha, F., Graves, C., Altitinchi, A., Farhadi, S. A., Macias, S. L., Wanchoo, A., Hudalla, G. A., Keselowsky, B. G., Wallet, S. M.. 2021-07-28. Submandibular Injection of Indoleamine 2,3-Dioxygenase Galectin-3 Fusion Protein Inhibits and Prevents Periodontal Disease Progression Over 12 Weeks. https://doi.org/10.1101/2021.07.28.454186

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

ATF3 Preserves Macrophage Cholesterol Homeostasis during Metabolic Stress

Background: Macrophages must coordinate immune activation with maintenance of cellular cholesterol homeostasis, yet the transcriptional mechanisms integrating these processes remain incompletely understood. Activating transcription factor 3 (ATF3) suppresses inflammatory and interferon responses and has been implicated in macrophage lipid metabolism, suggesting a role in coordinating immune and sterol-responsive transcriptional programs. Methods: Wild-type and ATF3-deficient bone marrow-derived macrophages were analyzed by bulk RNA sequencing following Toll-like receptor stimulation and under conditions of sterol loading or depletion. Cholesterol content, cytokine production, and sterol-responsive gene expression were quantified. Human metabolic dysfunction-associated steatotic liver disease (MASLD) datasets and Kupffer cell-specific ATF3 knockout mice were used to assess disease relevance in vivo. Results: ATF3 deficiency enhanced inflammatory and interferon-responsive transcriptional programs while suppressing a sterol-responsive gene module enriched for SREBP2 target genes. This phenotype was conserved across diverse Toll-like receptor stimuli and accompanied by persistent Ch25h upregulation. Despite exhibiting elevated cellular cholesterol, ATF3-deficient macrophages retained transcriptional responsiveness to sterol loading and depletion while demonstrating reduced induction of SREBP2-dependent genes across conditions. IFNAR blockade reduced interferon-responsive gene expression but did not normalize Ch25h or sterol-responsive gene expression. In contrast, CRISPR-mediated reduction of Ch25h partially restored sterol-responsive gene expression in inflammatory ATF3-deficient macrophages. In human MASLD, hepatic ATF3 expression positively correlated with disease severity. In mice, ATF3 was preferentially induced in Kupffer cells during metabolic stress, and Kupffer cell-specific deletion of ATF3 increased liver injury and Kupffer cell lipid accumulation. Conclusions: ATF3 supports sterol-responsive transcriptional programs while restraining inflammatory activation in macrophages. ATF3 loss results in elevated cellular cholesterol, impaired SREBP2-dependent gene expression, and persistent derepression of Ch25h, which contributes to but does not fully explain the sterol phenotype. These findings identify ATF3 as a coordinator of macrophage adaptation to inflammatory and metabolic stress and support a protective role for Kupffer cell ATF3 during metabolic liver disease.

immunology↗

Therapeutic anti-IgE antibodies generate distinct functional immune complex signatures

Therapeutic IgG anti-IgE antibodies are benchmarked by their ability to interfere with IgE-Fc[epsilon]RI binding, but their activity within IgE and IgG-containing immune complexes remains poorly defined. Here we show that omalizumab and ligelizumab form binary IgE-IgG and ternary allergen-containing immune complexes with distinct functional properties. In primary human leukocytes, these complexes exhibited antibody- and composition-dependent patterns of cellular association and activation. Using multiplexed focal molography, we resolved Fc receptor engagement across free and complexed antibody states and identified distinct receptor-binding signatures for omalizumab- and ligelizumab-containing complexes. Notably, allergen incorporation reversed the relative ability of the two antibodies to neutralize IgE-Fc[epsilon]RI interactions and remodelled Fc[gamma]R binding. Thus, immune-complex composition is a determinant of therapeutic antibody function.

immunology↗

Proliferation and mutation as humoral immune response

The affinity maturation process, through which antibodies acquire relatively high affinity for an invading pathogen, involves complex mechanisms whose relative importance is not yet fully understood. This study proposes an analytical model of this process, to investigate the main factors governing proliferation and mutation and assess their respective roles. The model suggests that the immune system should not be expected to follow a single, rigid evolutionary pattern, as a wide range of proliferation and mutation strategies can yield nearly optimal outcomes. Keywords: Antibody, antigen, affinity, B-cell, mutation, proliferation

immunology↗