….An unhealthy microbiome in the mother can make her unborn offspring susceptible to neurodevelopmental disorders. The researchers found that the IL-17a molecule was a key contributor to the development of autism-like symptoms in lab mice.
The good news is that the microbiome can be easily changed, either through diet, probiotic supplements or fecal transplant. All of these approaches seek to restore a healthy equilibrium among the different microorganisms that live in the gut.
“In terms of translating our work to humans, I think the next big step would be to identify features of the microbiome in pregnant mothers that correlate with autism risk,” Lukens said. “I think the really important thing is to figure out what kind of things can be used to modulate the microbiome in the mother as effectively and safely as we can.”
Blocking IL-17a also might offer a way to prevent autism, but it carries much more risk.
“If you think about pregnancy, the body is basically accepting foreign tissue, which is a baby,” said Lukens. “As a result, maintenance of embryonic health demands a complex balance of immune regulation, so people tend to shy away from manipulating the immune system during pregnancy.”.....
But, isn’t vaccinating, manipulating the immune system? We will discuss that more.
Now some may say, when will researchers finally stop blaming mothers for autism? Since the days of Refrigerator Mothers, mothers have had blame thrust upon them when it comes to a diagnosis of autism. Now, it is important to look at the ways a child’s microbiome may become dysfunctional and spiral into autism but is this idea of mom’s gut a true contributor? Some may say it’s a way to distract from the “environmental” sources of immune dysfunction we seem to be catapulted into these days. Let’s take a look.
Eating yogurt, taking probiotics, and eating healthy, organic foods are important but is that it? Not doing that causes autism? You may find it interesting that other research describes the importance of the postnatal infant microbiome :
Although intestinal bacterial colonization begins when a fetus is in the lower uterus, an infant's gut microbiota is established after birth. The establishment of a stable gut microbiota generally accompanies two big transitions in infancy. The first transition occurs soon after birth, during lactation, and results in dominance of the gut microbiota by Bifidobacterium. The second transition occurs during the weaning period, with the introduction of solid foods and continuation of breast milk feeding,17, 18, 19, 20, 21 and results in the establishment of an adult-type complex microbiome dominated by the phyla Bacteroidetes and Firmicutes. These alterations continue until three years of age …..
It is probably more accurate to say that a baby may get some of mom’s bacteria from birth...but it is not from her gut, but from her vagina or skin…….and we need to stress that AFTER BIRTH, the microbiota is established.
Interestingly, the gut microbiota of a newborn will closely resemble the microbiota that it encountered during birth. In vaginally delivery infants, gut microbiotas resemble their mothers' vaginal microbiotas, which are dominated by Lactobacillus, Prevotella, or Sneathia, whereas the microbiotas of infants born by caesarean section are most similar to skin microbiota, which is dominated by Staphylococcus, Corynebacterium, and Propionibacterium…..
Another thing that may have you wondering is this connection…..Vaccine Papers- An Objective Look at Vaccine Dangers : New Kid On The Block: IL-17a
An important new paper (January 2016) by Choi et al. in the well-known journal Science provides valuable new information about how IL-6 causes autism. This paper reports that IL-6 causes autism by inducing production of the cytokine IL-17a.
In biochemistry and biology, there are “signalling pathways” that have multiple steps connected in a chain. There can be many steps in a signaling pathway. Cytokines often act this way. So, when we say that “IL-6 causes autism”, it could mean that IL-6 acts directly, or that the IL-6 triggers something else that causes autism.
The new discovery is that IL-17a acts downstream of IL-6 to cause autism. In other words, IL-17a production is an intermediate step between IL-6 production and autism. So, Choi et al provides both a confirmation and extension of IL-6-autism causality.
This too, then about Thimerosal’s relationship to IL-6, could be considered as well, especially since pregnant women are told to get influenza vaccines:
A practical implication of the present findings has relevance to the commercial uses of THI as an antimicrobial agent in vaccines and consumer products because they identify DCs [dendritic cells] as sensitive targets for THI- and EtHg-mediated dysfunction. Given the importance of DCs as a front line in regulating lymphocyte mediated immunity and tolerance, altering DC functions by forms of EtHg should be considered when assessing contributions to altered immune function. In studies using the autoimmune-susceptible A.SW (H-2s ) mouse strain, THI induces a syndrome that is stronger and more generally manifested than those produced by methylmercury (Havarinasab et al. 2004), and development of autoimmunity in H-2s mice is dependent on cellular (T cell) and soluble (IFN-γ and IL-6) factors ………
It appears that there is more to this IL-17a connection and parents deserve the entire story.
Another important consideration is postnatal vaccination, as it appears that vaccination plays a big part in IL-17a production. It has to do with pathogens, memory immune responses, yet also can be a double-edged sword. Can that be important in autism research?
From CHOP, Children’s Hospital of Philadelphia, 2010: Th17 cytokines and Vaccine Induced Immunity
Recent compelling evidence has clearly changed this traditional paradigm of Th1/Th2 cell dichotomy to include a third subset of CD4 T cells referred to as T helper 17(Th17) cells[35, 52, 82]. Th17 cells produce the cytokines IL-17A (IL-17)....Importantly, the emerging evidence that Th17 cells are crucial players in generation of vaccine-induced protective responses against a variety of pathogens suggests that the incorporation of this knowledge into the design of current and future vaccines against infectious diseases will be a fruitful area of future research. It is also becoming apparent that the fine balance between protection and pathological manifestations of Th17 responses will define the final outcome of vaccine-induced IL-17 responses. Understanding the mechanism of induction and maintenance of IL-17 vaccine-induced responses has the potential to substantially impact vaccine strategies against infectious diseases.
Then we have autism -
Th17 cells have been implicated in the pathogenesis of autoimmune disease, findings supported by recent clinical trials using anti-IL-17 in the treatment of these diseases . Th17 cells are characterized by their production of IL-17 cytokines,
Autoimmunity to brain tissue may play a pathogenic role in autism. IL-17A is a pro-inflammatory cytokine that has been shown to play an important role in various autoimmune neuroinflammatory diseases. The aim of this study was to measure serum levels of IL-17A in relation to the degree of the severity of autism.
Children with autism had significantly higher serum IL-17A levels than healthy controls (P <0.001(Table 1, Figure 1). Increased serum IL-17A levels were found in 48.9% (22/45) of the patients with autism.
Patients with severe autism had significantly higher serum IL-17A levels than children with mild to moderate autism (P = 0.01) (Table 1, Figure 2), and the frequency of increased serum IL-17A levels was significantly higher in children with severe autism (19/28; 67.9%) than in patients with mild to moderate autism (3/17; 17.6%) (P = 0.001).
As we can see, the role of IL-17a appears significant in autism but the true source, mom’s gut vs vaccination, needs to be acknowledged.