On 2014 Jan 06, Paul Whiteley commented:

As per the science and lay media interest in this research at publication, this paper potentially opens up a whole new world of investigations looking at the interplay between the gastrointestinal (GI) tract and brain in respect to lots of different behaviourally-defined conditions. That being said, mouse models of autism still have some way to go to 'mimic' the complexity that is autism (even the 'autisms' according to Whitehouse & Stanley 2013: http://www.ncbi.nlm.nih.gov/pubmed/23545020) and the often substantial risk of heightened comorbidity of various types that follow a diagnosis.

Perhaps to some degree lost in the media translation of this research was the effect that B. fragilis administration seemed to have on gut barrier integrity (and in particular that B. fragilis "improves defects in GI barrier integrity and corrects alterations in tight junction and cytokine expression" p.1454). The notion of a triad of factors: gut barrier - gut microbiota - gut immune function is an important emerging concept in at least some autism research circles; these issues similarly being pursued in other research for example, linked to schizophrenia: Severance et al (2012) http://www.ncbi.nlm.nih.gov/pubmed/22446142

That there may specific types of autism which carry various GI issues including those related to issues with gut flora: Williams et al (2011) http://www.ncbi.nlm.nih.gov/pubmed/21949732 is another emerging concept with some potentially important knock-on effects: Stilling et al (2013) http://www.ncbi.nlm.nih.gov/pubmed/24286462.

Indeed, again drawing on other rodent models thought to reflect some of the complexity of autism, there is increasing understanding that GI issues may also for example, be present in the valproic acid (VPA) model as per the work from de Theije and colleagues (2013) http://www.ncbi.nlm.nih.gov/pubmed/24321212 and Kim and colleagues (2013) http://www.ncbi.nlm.nih.gov/pubmed/24386517.

Further that those with genetic conditions which present with autistic symptoms such as 22q11.2 deletion syndrome might also experience similar GI issues including those related to intestinal permeability as per the work of Giardino and colleagues (2013) http://www.ncbi.nlm.nih.gov/pubmed/24344832 is testament to the fact that further research resources are required to probe this potentially very interesting gut-brain interface.

On 2014 Jan 06, Paul Whiteley commented:

As per the science and lay media interest in this research at publication, this paper potentially opens up a whole new world of investigations looking at the interplay between the gastrointestinal (GI) tract and brain in respect to lots of different behaviourally-defined conditions. That being said, mouse models of autism still have some way to go to 'mimic' the complexity that is autism (even the 'autisms' according to Whitehouse & Stanley 2013: http://www.ncbi.nlm.nih.gov/pubmed/23545020) and the often substantial risk of heightened comorbidity of various types that follow a diagnosis.

Perhaps to some degree lost in the media translation of this research was the effect that B. fragilis administration seemed to have on gut barrier integrity (and in particular that B. fragilis "improves defects in GI barrier integrity and corrects alterations in tight junction and cytokine expression" p.1454). The notion of a triad of factors: gut barrier - gut microbiota - gut immune function is an important emerging concept in at least some autism research circles; these issues similarly being pursued in other research for example, linked to schizophrenia: Severance et al (2012) http://www.ncbi.nlm.nih.gov/pubmed/22446142

That there may specific types of autism which carry various GI issues including those related to issues with gut flora: Williams et al (2011) http://www.ncbi.nlm.nih.gov/pubmed/21949732 is another emerging concept with some potentially important knock-on effects: Stilling et al (2013) http://www.ncbi.nlm.nih.gov/pubmed/24286462.

Indeed, again drawing on other rodent models thought to reflect some of the complexity of autism, there is increasing understanding that GI issues may also for example, be present in the valproic acid (VPA) model as per the work from de Theije and colleagues (2013) http://www.ncbi.nlm.nih.gov/pubmed/24321212 and Kim and colleagues (2013) http://www.ncbi.nlm.nih.gov/pubmed/24386517.

Further that those with genetic conditions which present with autistic symptoms such as 22q11.2 deletion syndrome might also experience similar GI issues including those related to intestinal permeability as per the work of Giardino and colleagues (2013) http://www.ncbi.nlm.nih.gov/pubmed/24344832 is testament to the fact that further research resources are required to probe this potentially very interesting gut-brain interface.