Corrigendum: Evaluation of the efficacy of humic acids to counteract the toxic effects of aflatoxin B1 in turkey poults.

[This corrects the article DOI: 10.3389/fvets.2023.1276754.].

Evaluation of the efficacy of humic acids to counteract the toxic effects of aflatoxin B1 in turkey poults.

This study aims to evaluate the efficacy of humic acid (HA) from worm compost as an adsorbent for aflatoxin B1 (AFB1) in turkey poults. The experiment involved the inclusion of 0.25% (w/w) HA in the diet of turkey poults consuming aflatoxin-contaminated feed (250 ng AFB1/g). A total of 350 1-day-old female Nicholas-700 turkey poults were randomly allocated to five equal groups: negative control (basal diet); positive control (basal diet + 250 ng AFB1/g; HA (basal diet + 0.25% HA); HA + AFB1 (basal diet + HA + 250 ng AFB1/g); and zeolite + AFB1 (basal diet + 0.25% zeolite + 250 ng AFB1/g). Each group had seven replicates of 10 poults (n = 70). The impact of HA addition was evaluated in terms of performance parameters, relative organ weights, liver histological lesions, and serum biochemical and hematological constituents. In general, the addition of HA improved body weight (BW), body weight gain (BWG), and feed conversion rate (FCR). Furthermore, HA effectively mitigated the toxic effects caused by AFB1 in the majority of the analyzed variables. The results indicated that HA effectively counteracted the AFB1-induced toxic effects in turkey poults. Based on these findings, it can be concluded that HA is capable of removing AFB1 from the contaminated diet.

Mitigation of AFB1-Related Toxic Damage to the Intestinal Epithelium in Broiler Chickens Consumed a Yeast Cell Wall Fraction.

In vivo experiments were conducted to evaluate the effectiveness of a yeast cell wall fraction (YCW) to reduce the negative impact of aflatoxin B1 (AFB1) to the intestinal epithelium in broiler chickens. Zeta potential (ζ-potential), point of zero charge (pHpzc), Fourier transform infrared spectroscopy (FTIR), and scanning electron microscopy (SEM) techniques were used to characterize the YCW. Two hundred one-day-old male Ross 308 broiler chickens were randomly allocated into four treatments: (1) control, chickens fed an AFB1-free diet; (2) AF, chickens feed an AFB1-contaminated diet (500 ng AFB1/g); (3) YCW, chickens fed an AFB1-free diet + 0.05% YCW; and (4) AF + YCW, chickens fed an AFB1-contaminated diet (500 ng AFB1/g) + 0.05% YCW. At the end of the 21-day feeding period, fluorescein isothiocyanate dextran (FITC-d) was administered to chicks by oral gavage to evaluate gastrointestinal leakage. Blood and duodenum samples were collected to assess serum biochemistry and histomorphology, respectively. Compared to the control group, chicks of the AF group significantly diminished weight gain (WG) and average daily feed intake (ADFI), and increased feed conversion ratio (FCR), mortality rate (MR), and intestinal lesion scores (p < 0.05). Alterations in some serum biochemical parameters, and damage to the intestinal integrity were also evident in the AF-intoxicated birds. YCW supplementation improved WG and FCR and increased villus height, villus area, crypt depth, and the number of goblet cells in villi. The effects of YCW on growth performance were not significant in chicks of the AF + YCW group; however, the treatment decreased MR and significantly ameliorated some biochemical and histomorphological alterations. The beneficial effect of YCW was more evident in promoting gut health since chickens of the AF + YCW group presented a significant reduction in serum FITC-d concentration. This positive effect was mainly related to the changes in negative charges of YCW due to changes in pH, the net negative surface charge above the pHpzc, the higher quantities of negative charged functional groups on the YCW surface, and its ability to form large aggregates. From these results, it can be concluded that YCW at low supplementation level can partially protect broilers' intestinal health from chronic exposure to AFB1.

Lactoferrin and Its Derived Peptides: An Alternative for Combating Virulence Mechanisms Developed by Pathogens.

Due to the emergence of multidrug-resistant pathogens, it is necessary to develop options to fight infections caused by these agents. Lactoferrin (Lf) is a cationic nonheme multifunctional glycoprotein of the innate immune system of mammals that provides numerous benefits. Lf is bacteriostatic and/or bactericidal, can stimulate cell proliferation and differentiation, facilitate iron absorption, improve neural development and cognition, promote bone growth, prevent cancer and exert anti-inflammatory and immunoregulatory effects. Lactoferrin is present in colostrum and milk and is also produced by the secondary granules of polymorphonuclear leukocytes, which store this glycoprotein and release it at sites of infection. Lf is also present in many fluids and exocrine secretions, on the surfaces of the digestive, respiratory and reproductive systems that are commonly exposed to pathogens. Apo-Lf (an iron-free molecule) can be microbiostatic due to its ability to capture ferric iron, blocking the availability of host iron to pathogens. However, apo-Lf is mostly microbicidal via its interaction with the microbial surface, causing membrane damage and altering its permeability function. Lf can inhibit viral entry by binding to cell receptors or viral particles. Lf is also able to counter different important mechanisms evolved by microbial pathogens to infect and invade the host, such as adherence, colonization, invasion, production of biofilms and production of virulence factors such as proteases and toxins. Lf can also cause mitochondrial and caspase-dependent regulated cell death and apoptosis-like in pathogenic yeasts. All of these mechanisms are important targets for treatment with Lf. Holo-Lf (the iron-saturated molecule) can contain up to two ferric ions and can also be microbicidal against some pathogens. On the other hand, lactoferricins (Lfcins) are peptides derived from the N-terminus of Lf that are produced by proteolysis with pepsin under acidic conditions, and they cause similar effects on pathogens to those caused by the parental Lf. Synthetic analog peptides comprising the N-terminus Lf region similarly exhibit potent antimicrobial properties. Importantly, there are no reported pathogens that are resistant to Lf and Lfcins; in addition, Lf and Lfcins have shown a synergistic effect with antimicrobial and antiviral drugs. Due to the Lf properties being microbiostatic, microbicidal, anti-inflammatory and an immune modulator, it represents an excellent natural alternative either alone or as adjuvant in the combat to antibiotic multidrug-resistant bacteria and other pathogens. This review aimed to evaluate the data that appeared in the literature about the effects of Lf and its derived peptides on pathogenic bacteria, protozoa, fungi and viruses and how Lf and Lfcins inhibit the mechanisms developed by these pathogens to cause disease.