Antibiotics and steroids, the double enemies of anticancer immunotherapy: a review of the literature
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REVIEW
Antibiotics and steroids, the double enemies of anticancer immunotherapy: a review of the literature Fausto Meriggi1 · Alberto Zaniboni1 Received: 16 June 2020 / Accepted: 27 October 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract The advent of immunotherapy in onco-haematology has represented a kind of revolution that has been able to modify the prognosis of numerous tumours that until recently would have been rapidly lethal. While much is known about the mechanism of action of these drugs, relatively little is known about the factors that represent potential predictors of response and toxicity. Among these factors, the simultaneous administration of antibiotics and/or steroids seems to have a negative impact. Furthermore, several retrospective studies have highlighted the strong link between cancer and gut microbiota, regardless of the tumour site, and how microbiota, playing a key role in the prevention of systemic inflammation at various levels and in the intestinal homeostasis, can be negatively influenced by the dysbiosis caused by antibiotic therapy administered during or in the weeks immediately preceding the start of immunotherapy. Moreover, we assume that the concurrent administration of steroids, which is often necessary in cancer patients, likely results in a deleterious effect on the therapeutic outcomes of immunotherapy. In this review, we will try to clarify the evidence on the possible detrimental effects of antibiotics and steroids, which are currently considered the double enemies of anticancer immunotherapy. Keywords Immunotherapy · Antibiotic therapy · Gut microbiota · Corticosteroids
Introduction The advent and development of new cancer treatments such as immunotherapy (IO) have led to significant improvements, especially for some patients who have been able to benefit from or experience dramatic and lasting responses, even in advanced cancers that until a few years ago were considered to have a bad prognosis with extremely short survival times. The main mechanism of action of the immune checkpoint inhibitors (ICIs) consists of reversing the blockade of the inhibitory effect between the T lymphocyte receptor and its ligand located on neoplastic cells or myeloid cells, thus allowing the T lymphocyte-mediated response against tumour antigens. ICIs are monoclonal antibodies (mAbs) that target PD-1 (programmed cell death-1) and PD-L1 (programmed cell death ligand-1) or target cytotoxic * Fausto Meriggi [email protected] Alberto Zaniboni [email protected] 1
Oncology Department, Poliambulanza Foundation, Via Leonida Bissolati 57, 25124 Brescia, Italy
T-lymphocyte antigen 4 (CTLA-4), which act to enable cytotoxic lymphocytes to regain their ability to attack tumour cells [1]. However, the magnitude of the responses and the spectrum of toxicities to IO are still extremely variable, and further research is needed to identify more reliable predictive factors, particularly those concerning the host. A refractoriness to ICIs is present, depending on study, in
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